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1. Huang D, Sumegi J, Dal Cin P, Reith JD, Yasuda T, Nelson M, Muirhead D, Bridge JA: C11orf95-MKL2 is the resulting fusion oncogene of t(11;16)(q13;p13) in chondroid lipoma. Genes Chromosomes Cancer; 2010 Sep;49(9):810-8
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  • [Title] C11orf95-MKL2 is the resulting fusion oncogene of t(11;16)(q13;p13) in chondroid lipoma.
  • Chondroid lipoma, a rare benign adipose tissue tumor, may histologically resemble myxoid liposarcoma or extraskeletal myxoid chondrosarcoma, but is genetically distinct.
  • In this study, an identical reciprocal translocation, t(11;16)(q13;p13), was identified in three chondroid lipomas, a finding consistent with previously isolated reports.

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
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  • (PMID = 20607705.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA036727-24S59009; United States / NCI NIH HHS / CA / 5 P30 CA036727-2452; United States / NCI NIH HHS / CA / P30 CA036727-24S59009; United States / NCI NIH HHS / CA / U-10-CA98543-091
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MKL2 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS203810; NLM/ PMC2904421
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2. Svegliati-Baroni G, Candelaresi C, Saccomanno S, Ferretti G, Bachetti T, Marzioni M, De Minicis S, Nobili L, Salzano R, Omenetti A, Pacetti D, Sigmund S, Benedetti A, Casini A: A model of insulin resistance and nonalcoholic steatohepatitis in rats: role of peroxisome proliferator-activated receptor-alpha and n-3 polyunsaturated fatty acid treatment on liver injury. Am J Pathol; 2006 Sep;169(3):846-60
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  • [Title] A model of insulin resistance and nonalcoholic steatohepatitis in rats: role of peroxisome proliferator-activated receptor-alpha and n-3 polyunsaturated fatty acid treatment on liver injury.
  • Insulin resistance induces nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH).
  • We used a high-fat, high-calorie solid diet (HFD) to create a model of insulin resistance and NASH in nongenetically modified rats and to study the relationship between visceral adipose tissue and liver.
  • Obesity and insulin resistance occurred in HFD rats, accompanied by a progressive increase in visceral adipose tissue tumor necrosis factor (TNF)-alpha mRNA and in circulating free fatty acids.
  • HFD also decreased adiponectin mRNA and peroxisome proliferator-activated receptor (PPAR)-alpha expression in the visceral adipose tissue and the liver, respectively, and induced hepatic insulin resistance through TNF-alpha-mediated c-Jun N-terminal kinase (JNK)-dependent insulin receptor substrate-1Ser307 phosphorylation.
  • Supplementation of n-3 polyunsaturated fatty acid, a PPARalpha ligand, to HFD-treated animals restored hepatic adiponectin and PPARalpha expression, reduced TNF-alpha hepatic levels, and ameliorated fatty liver and the degree of liver injury.
  • Thus, our model mimics the most common features of NASH in humans and provides an ideal tool to study the role of individual pathogenetic events (as for PPARalpha down-regulation) and to define any future experimental therapy, such as n-3 polyunsaturated fatty acid, which ameliorated the degree of liver injury.
  • [MeSH-major] Fatty Acids, Omega-3 / metabolism. Fatty Liver / metabolism. Insulin Resistance. Intra-Abdominal Fat / metabolism. Liver / metabolism
  • [MeSH-minor] Animals. Apoptosis. Disease Models, Animal. Down-Regulation. Fibrosis / metabolism. Fibrosis / pathology. Food, Formulated / adverse effects. Hepatocytes / metabolism. Hepatocytes / pathology. Humans. Insulin Receptor Substrate Proteins. JNK Mitogen-Activated Protein Kinases / metabolism. Male. Necrosis / metabolism. Necrosis / pathology. Oxidative Stress. Phosphoproteins / metabolism. Protein Processing, Post-Translational. RNA, Messenger / biosynthesis. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 16936261.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Omega-3; 0 / IRS1 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / Irs1 protein, rat; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1698833
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3. Zemel MB, Sun X: Dietary calcium and dairy products modulate oxidative and inflammatory stress in mice and humans. J Nutr; 2008 Jun;138(6):1047-52
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  • Accordingly, this study was designed to study the effects of the short-term (3 wk) basal suboptimal Ca (0.4%), high-Ca (1.2% from CaCO(3)), and high-dairy (1.2% Ca from milk) obesigenic diets on oxidative and inflammatory stress in adipocyte fatty acid-binding protein-agouti transgenic mice.
  • Adipose tissue reactive oxygen species (ROS) production and NADPH oxidase mRNA and plasma malondialdehyde (MDA) were reduced by the high-Ca diet (P < 0.001) compared with the basal diet and ROS and MDA were further decreased by the high-dairy diet (P < 0.001).
  • The high-Ca and -dairy diets also resulted in suppression of adipose tissue tumor necrosis factor alpha and interleukin (IL)-6 mRNA (P = 0.001) compared with the basal diet, whereas an inverse pattern was noted for adiponectin and IL-15 mRNA (P = 0.002).
  • These data demonstrate that dietary Ca suppresses adipose tissue oxidative and inflammatory stress.

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  • (PMID = 18492832.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Calcium, Dietary; 0 / Dietary Carbohydrates; 0 / Dietary Fats; 9007-41-4 / C-Reactive Protein
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4. Arikawa S, Uchida M, Shinagawa M, Tohnan T, Hayabuchi N: Significance of the " beak sign"in the differential diagnosis of uterine lipoleiomyoma from ovarian dermoid cyst. Kurume Med J; 2006;53(1-2):37-40
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  • [Title] Significance of the " beak sign"in the differential diagnosis of uterine lipoleiomyoma from ovarian dermoid cyst.
  • Although a series of imaging studies suggested a lipomatous tumor, diagnosis was difficult because the tumor appeared as a pedunculated mass extending from the uterine body.
  • To distinguish the tumor from an ovarian lipomatous tumor, the "beak sign" in a magnetic resonance imaging study was diagnostic in this case.
  • The purpose of this paper is to review lipomatous masses of the female pelvis, to discuss the differential diagnosis of the unusual imaging features, and to discuss imaging techniques to optimize pelvic mass characterization.
  • [MeSH-major] Leiomyoma / diagnosis. Lipoma / diagnosis. Ovarian Cysts / diagnosis. Uterine Neoplasms / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging. Tomography, X-Ray Computed

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  • (PMID = 17043394.001).
  • [ISSN] 0023-5679
  • [Journal-full-title] The Kurume medical journal
  • [ISO-abbreviation] Kurume Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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5. Gurel D, Kargi A, Lebe B: Pedunculated cutaneous spindle cell/pleomorphic lipoma. J Cutan Pathol; 2010 Sep;37(9):e57-9
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  • Spindle cell/pleomorphic lipoma is an infrequently seen benign adipose tissue tumor.
  • This tumor, mostly arising from the subcutaneous tissue, usually affects male patients and occurs in back, shoulders, head and neck area.
  • [MeSH-major] Lipoma / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Antigens, CD34 / metabolism. Biomarkers, Tumor / metabolism. Dermis / pathology. Humans. Male. Vimentin / metabolism

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  • (PMID = 19678825.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / Vimentin
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6. An JJ, Han DH, Kim DM, Kim SH, Rhee Y, Lee EJ, Lim SK: Expression and regulation of osteoprotegerin in adipose tissue. Yonsei Med J; 2007 Oct 31;48(5):765-72
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  • [Title] Expression and regulation of osteoprotegerin in adipose tissue.
  • Adipocytes and osteoblasts share a common origin, and the formation of new blood vessels often precedes adipogenesis in developing adipose tissue microvasculature.
  • MATERIALS AND METHODS: The mRNA expression of OPG and receptor activator of NF-kappaB ligand (RANKL) was measured in differentiated 3T3L1 adipocytes and adipose tissues.
  • RESULTS: OPG mRNA expression increased with the differentiation of 3T3L1 adipocytes, while RANKL expression was not significantly altered.
  • OPG mRNA was expressed at higher levels in white adipose tissue than in brown adipose tissue and was most abundant in the epididymal portion.
  • In contrast, tumor necrosis factor-alpha (TNF-alpha) increased the expression of both OPG and RANKL in a time-dependent manner.
  • CONCLUSION: Our results indicate that OPG mRNA is expressed and regulated in the adipose tissue.
  • Considering the role of OPG in obesity-associated inflammatory changes in adipose tissue and vessels, we speculate that OPG may have both a protective function against inflammation and anti-angiogenic effects on adipose tissue.
  • [MeSH-major] Adipose Tissue / metabolism. Gene Expression Regulation. Osteoprotegerin / metabolism
  • [MeSH-minor] 3T3-L1 Cells. Adipocytes / cytology. Adipocytes / drug effects. Adipocytes / metabolism. Adipogenesis / genetics. Animals. Cell Differentiation. Hypoglycemic Agents / pharmacology. Insulin / pharmacology. Male. Mice. RANK Ligand / metabolism. Rats. Rats, Sprague-Dawley. Thiazolidinediones / pharmacology. Transfection. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 17963332.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Insulin; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Thiazolidinediones; 0 / Tnfrsf11b protein, mouse; 0 / Tnfsf11 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 05V02F2KDG / rosiglitazone
  • [Other-IDs] NLM/ PMC2628141
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7. Poon E, Verhaegen F: Sci-Sat AM(2): Brachy-08: Monte Carlo calculations of 192Ir high dose rate brachytherapy treatment plans using CT and cone beam CT images. Med Phys; 2008 Jul;35(7Part3):3417
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  • To evaluate the effects of tissue heterogeneities and finite patient dimensions for 192Ir high dose rate treatment, CT-based MC calculations for breast and head and neck cases were first performed using the PTRAN_CT photon transport code.
  • Muscles and adipose tissues, which are nearly indistinguishable in CBCT images, are found to cause minimal dose perturbations at 192Ir energies compared to water.
  • The proximity of the tumor to the skin, however, will have an observable impact on the dose up to a few percent.
  • A CBCT-based calculation for an actual treatment plan with the tumor close to the cheek was performed.
  • Since the dose delivered to the tumor is mostly primary dose, deviations are found mostly in the organs at risk where scatter contribution becomes more significant.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28512889.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Brachytherapy / Cancer / Computed tomography / Cone beam computed tomography / Dosimetry / Medical image quality / Medical imaging / Monte Carlo methods / Skin / Tissues
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8. Costa JV, Duarte JS: [Adipose tissue and adipokines]. Acta Med Port; 2006 May-Jun;19(3):251-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adipose tissue and adipokines].
  • [Transliterated title] Tecido adiposo e adipocinas.
  • Adipose tissue is an organ with an endocrine function among others.
  • Interleukin-6, tumour necrosis factor a and complement factors B, C3 and D (adipsin) and are within the first group.
  • Adipose tissue is mainly involved in lipid and glucose metabolism.
  • Free fatty acids, adiponectin, resistin, agouti related peptide and visfatin are molecules involved in those metabolic pathways.
  • Leptin is the paradigm of the adipose tissue endocrine function.
  • Steroid inter-conversion also occurs in adipose tissue.
  • [MeSH-major] Complement System Proteins / physiology. Interleukin-6 / physiology. Subcutaneous Fat / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 17234088.001).
  • [ISSN] 1646-0758
  • [Journal-full-title] Acta médica portuguesa
  • [ISO-abbreviation] Acta Med Port
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Portugal
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 9007-36-7 / Complement System Proteins
  • [Number-of-references] 17
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9. Fernández-Sueiro JL, Pinto JA, Blanco FJ, Freire M, Veiga JA, Galdo F, González-Gay MA: Multiple parosteal lipoma associated to polyarthritis. Joint Bone Spine; 2006 Mar;73(2):202-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Parosteal lipoma is a benign adipose tissue tumor situated directly in the bone cortex.
  • We describe a patient who presented with polyarthritis associated with multiple parosteal lipomatous involvement.
  • A tissue sample from the distal portion of the forearm confirmed the presence of cumulative fat tissue with nodes of esteatonecrosis.
  • [MeSH-major] Arthritis / etiology. Bone Neoplasms / complications. Lipoma / complications. Periosteum / pathology
  • [MeSH-minor] Adipose Tissue / pathology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Drug Therapy, Combination. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Prednisone / therapeutic use. Tomography, X-Ray Computed. Wrist / pathology. Wrist / radiography

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  • (PMID = 16226479.001).
  • [ISSN] 1297-319X
  • [Journal-full-title] Joint, bone, spine : revue du rhumatisme
  • [ISO-abbreviation] Joint Bone Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; VB0R961HZT / Prednisone
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10. Nishida J, Ehara S, Shiraishi H, Tada H, Satoh T, Okada K, Shimamura T: Clinical findings of hibernoma of the buttock and thigh: rare involvements and extremely high uptake of FDG-PET. Med Sci Monit; 2009 Jul;15(7):CS117-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Hibernoma is a rare adipose tissue tumor of the soft tissue and the term is derived from the histological similarities to the brown fat found in hibernating animals.
  • This was not typical of liposarcoma and suggestive of hibernoma.
  • Biopsy specimens revealed a proliferation of adipose cells with vacuolated granular eosinophilic cytoplasm.
  • CONCLUSIONS: While occurrences in the buttock or thigh are exceedingly rare, hibernoma should be included in the differential diagnosis of an adipose tissue tumor in the thigh, even though the imaging findings mimic liposarcoma.
  • A correct diagnosis should be established to prevent over-surgery.

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  • (PMID = 19564831.001).
  • [ISSN] 1643-3750
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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11. Italiano A, Chambonniere ML, Attias R, Chibon F, Coindre JM, Pedeutour F: Monosomy 7 and absence of 12q amplification in two cases of spindle cell liposarcomas. Cancer Genet Cytogenet; 2008 Jul 15;184(2):99-104

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Spindle cell liposarcoma (SCL) is a rare malignant adipose tissue tumor presently regarded as a variant of well-differentiated liposarcoma (WDLPS).
  • In these two cases, we did not identify supernumerary ring or giant chromosomes containing 12q amplification or any other chromosome 12 rearrangement.
  • Monosomy 7 is not usual in adipose tissue tumors.
  • It has been described in myelodysplastic syndromes and acute myeloid or lymphoblastic leukemias, as well as in several benign or malignant solid tumors.
  • Our data suggest that the loss of material from chromosome 7 might play a crucial role in the pathogenesis of some SCL probably through the inactivation of tumor suppressor genes located on chromosome 7.
  • [MeSH-major] Carcinoma / genetics. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Gene Amplification. Liposarcoma / genetics. Monosomy / diagnosis

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  • (PMID = 18617058.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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12. Speer AL, Schofield DE, Wang KS, Shin CE, Stein JE, Shaul DB, Mahour GH, Ford HR: Contemporary management of lipoblastoma. J Pediatr Surg; 2008 Jul;43(7):1295-300
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Lipoblastoma is a rare, benign, adipose tissue tumor.
  • We report the largest single institution experience managing these uncommon neoplasms.
  • CONCLUSIONS: A staged approach with meticulous sparing of the neurovascular bundle provides excellent functional outcome for patients with large tumors.
  • [MeSH-major] Neoplasms, Adipose Tissue / surgery. Soft Tissue Neoplasms / surgery

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  • (PMID = 18639685.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Aust MC, Spies M, Kall S, Jokuszies A, Gohritz A, Vogt P: Posttraumatic lipoma: fact or fiction? Skinmed; 2007 Nov-Dec;6(6):266-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Lipomas are usually benign adipose tumors with as-yet unexplained pathogenesis and etiology.
  • A link between soft tissue trauma and the formation of lipomas has been described, with the latter being named posttraumatic lipomas.
  • The average time between soft tissue trauma and lipoma formation was 2.6 years (range, 0.5-6.0 years).
  • All tumors were located epifascially.
  • Pathology demonstrated capsulated and noncapsulated benign adipose tumors in 23 cases.
  • CONCLUSIONS: The pathogenetic link between soft tissue trauma and the formation of posttraumatic lipomas is still controversially discussed.
  • There are 2 potential explanations to correlate soft tissue trauma and adipose tissue tumor growth.
  • The first is the formation of so-called posttraumatic pseudolipomas by prolapsing adipose tissue through fascia resulting from direct impact.
  • A second possibility points toward lipoma formation as a result of preadipocyte differentiation and proliferation mediated by cytokine release following soft tissue trauma and hematoma formation.
  • [MeSH-major] Adipose Tissue / injuries. Lipoma / etiology. Neoplasms, Adipose Tissue / etiology. Wounds, Nonpenetrating / complications

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  • (PMID = 17975353.001).
  • [ISSN] 1540-9740
  • [Journal-full-title] Skinmed
  • [ISO-abbreviation] Skinmed
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Bilici A, Guler DO, Seker M, Ustaalioglu BO, Sonmez B, Karaduman M, Oncel M, Gumus M, Salepci T, Yaylaci M: The correlation among tissue, serum adiponectin levels and histopathological variables in gastric cancer patients. J Clin Oncol; 2009 May 20;27(15_suppl):e22199

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The correlation among tissue, serum adiponectin levels and histopathological variables in gastric cancer patients.
  • : e22199 Background: Adiponectin is a new peptide hormone secreted from the adipose tissue, affecting the proliferation and insulin sensitivity in different cell types.The previous studies showed that the serum levels of adiponectin are decreased in patients with endometrial and breast cancer.In our study, demographic features and histopathological variables and the relationship among adiponectin levels of serum and gastric tissue were analyzed in gastric cancer patients.
  • METHODS: Thirty-five consecutive patients with gastric cancer included in this study.The serum levels of glucose, insulin, c-peptide, HbA1c, lipids and adiponectin were measured in patients.In addition, normal and tumor tissue levels of adiponectin were also detected.We analyzed the correlation among these parameters and patients demographic features, such as age, gender, body mass index (BMI) and histopathological variables.
  • The mean serum, normal and tumor tissue levels of adiponectin were 49.4±0.8, 48.2±4.2, 48.6±2.9 ng/ml, respectively.
  • There was no relationship among serum, normal and tumor tissue adiponectin levels (p>0.05).There was inverse correlation between the normal tissue levels of adiponectin and insulin (p=0.002).The serum adiponectin levels were significantly associated with tumor localization (p=0.03).However, there was inverse correlation between serum adiponectin levels and perineural invasion (p=0.02).In subgroup analysis, the serum, normal and tumor tissue levels of adiponectin in woman were not different compared with those in male patients (p>0.05).No relations were detected among tumor stage, grade, nodal status, lymphatic and vascular invasion, the other insulin-resistant status parameters and the levels of serum, normal and tumor tissue adiponectin (p>0.05).
  • CONCLUSIONS: Our results suggest that no correlations among the levels of serum adiponectin,normal tissue and tumor tissue adiponectin levels,patients demographic features and histopathological variables except for the association of serum adiponectin with tumor localization and perineural invasion detected in gastric cancer patients.

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  • (PMID = 27963639.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Carroll PA, Healy L, Lysaght J, Griffin M, Dunne B, Boyle MT, Reynolds JV, Kennedy MJ, Pidgeon G, Connolly EM: Mammary adipose tissue and cancer cell growth: The role of adipose tissue in the tumor microenvironment. J Clin Oncol; 2009 May 20;27(15_suppl):e22009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammary adipose tissue and cancer cell growth: The role of adipose tissue in the tumor microenvironment.
  • Adipose tissue is considered an important endocrine organ producing several important hormones and cytokines including leptin and adiponectin.
  • Mechanisms for the role of obesity in cancer states includes the excess or unregulated secretion of adipocytokines from adipose tissue, and potentially the metabolic syndrome (a cluster of co-morbidities linked to metabolic dysregulation).
  • Mammary adipose tissue is proposed to play a vital role in the microenvironment of normal and tumour states within the breast<sup>2</sup>.
  • Breast adipose tissue is a good candidate to investigate effects of obesity and metabolic disturbances on cancer states.
  • METHODS: Peritumoural (PT) adipose tissue adjacent to the tumour and distal adipose tissue (D) within the breast was sampled in 10 patients.
  • The tissue was processed and cultured for 72hrs in serum free minimal cytokine media.
  • The adipocytokine profile at the mRNA and protein level was measured in ACM and adipose tissue for comparative differences using RT-PCR, ELISA and Cytokine Profiler technology.
  • RESULTS: ACM from both sites promoted tumour cell survival.
  • This may be mediated through increased pro-inflammatory or pro- mitogenic adipocytokine production in adipose tissue surrounding tumour.

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  • (PMID = 27963182.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Mineo JF, P-Ruchoux MM, Pasquier D, Rigolle H, Assaker R: [Primitive malignant melanoma arising in a spinal nerve root. A case report]. Neurochirurgie; 2006 Jun;52(2-3 Pt 1):133-7
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  • The T1-weighted MRI images showed a tumor hyperintensity, the T2-weighted images showed tumor isointensity and mild contrast enhancement.
  • Due to the scalloping of L3/L4 foramen with root enlargement and slow evolution (more than one year between the first symptom and surgery without clinical worsening), the initial preoperative diagnosis was L3 schwannoma.
  • The tumor was composed of irregular melanocytoid cells with high proliferation index (20%).
  • So, the final diagnosis was intradural primitive malignant melanoma.
  • Radiotherapy was performed on the site of the tumor.
  • The most common tumor with root enlargement and bony scalloping is the benign schwannoma.
  • Despite the above described radiological features, MRI characteristics (hyperintensity when images are T1-weighted) suggest a melanocytic tumor, a tumor with a high adipose component or an intratumoral bleeding.
  • Specific MRI sequences can eliminate adipose tissue tumor, but diagnosis between melanin and methemoglobin is still difficult.
  • These tumors show identical protein expressions in immunohistochemistry, and their prognosis is very variable (some long-term remissions are reported for malignant melanomas and fast disseminations are described for meningeal melanocytomas treated by sub-total surgery).
  • [MeSH-major] Melanoma / pathology. Spinal Neoplasms / pathology. Spinal Nerve Roots / pathology
  • [MeSH-minor] Adult. Antigens, Neoplasm. Cell Proliferation. Fatal Outcome. Female. Humans. Immunohistochemistry. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Melanins / metabolism. Melanoma-Specific Antigens. Neoplasm Proteins / metabolism. Neurologic Examination. S100 Proteins / metabolism

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  • (PMID = 16840974.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Melanins; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / S100 Proteins
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17. Obora A, Kojima T, Kato T, Matsuda H, Horie H, Hashimoto H, Fukuta N, Takano Y, Okuda J, Ida K, Saio M: [An autopsy case of hepatocellular carcinoma in which sarcoma-like changes and peritoneal dissemination were observed after RFA/TACE treatment]. Gan To Kagaku Ryoho; 2009 Jul;36(7):1183-6
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  • Liver biopsy led to a diagnosis of well-differentiated hepatocellular carcinoma.
  • CT revealed pleural effusion/ascites and nodular tumor in the adipose tissue of the parietal peritoneum and mesentery around the liver.
  • Autopsy revealed a tumor involving the liver surface to the peritoneum, suggesting cancerous peritonitis.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Catheter Ablation. Chemoembolization, Therapeutic. Liver Neoplasms / therapy

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  • (PMID = 19620814.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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18. Novikov VV, Novikov GV, Fesenko EE: Effect of weak combined static and extremely low-frequency alternating magnetic fields on tumor growth in mice inoculated with the Ehrlich ascites carcinoma. Bioelectromagnetics; 2009 Jul;30(5):343-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of weak combined static and extremely low-frequency alternating magnetic fields on tumor growth in mice inoculated with the Ehrlich ascites carcinoma.
  • It was shown that the exposure of mice with EAC to combined MFs causes structural changes in some organs (liver, adrenal glands), which are probably due to the total degradation of the tumor tissue.
  • In mice with transplanted EAC, the tumor tissue after exposure to weak MFs was practically absent, as distinct from control animals in which the invasion of the tumor into the adipose tissue surrounding the kidneys, mesenteric lymph nodes, and spermatic appendages was observed.
  • In animals without tumors, no pathological deviations from the norm in the structure of organs and tissues occurred after exposure to weak MF, indicating that this factor per se is not toxic to the organism.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / pathology. Carcinoma, Ehrlich Tumor / therapy. Magnetic Field Therapy / methods. Magnetics

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19267367.001).
  • [ISSN] 1521-186X
  • [Journal-full-title] Bioelectromagnetics
  • [ISO-abbreviation] Bioelectromagnetics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Marsilia GM, Boscaino A, La Mura A, Ceriello A, De Ritis R: Hepatic angiomyolipoma and intramural small intestinal schwannoma: a coincidence or a relationship? Int J Surg Pathol; 2010 Dec;18(6):537-9
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  • Histologically, hepatic angiomyolipoma showed oncocytic features and scanty adipose tissue, the tumor cells expressed desmin, smooth muscle actin, S-100 protein and HMB45.
  • The tumor cells of intramural small intestinal mass were positive for S-100 protein and GFAP and negative for CD117, CD34 and desmin.
  • [MeSH-major] Angiomyolipoma / pathology. Jejunal Neoplasms / pathology. Liver Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Neurilemmoma / pathology

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  • (PMID = 19282295.001).
  • [ISSN] 1940-2465
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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20. Kabasawa Y, Katsube K, Harada H, Nagumo K, Terasaki H, Perbal B, Okada N, Omura K: A male infant case of lipofibromatosis in the submental region exhibited the expression of the connective tissue growth factor. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2007 May;103(5):677-82
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  • [Title] A male infant case of lipofibromatosis in the submental region exhibited the expression of the connective tissue growth factor.
  • METHODS: We examined morphological aspects of the tumor and immunohistochemical patterns.
  • RESULTS: Tumor proliferation was infiltrative, which did not show apparent encapsulation.
  • Positive immunoreactivity was found for CD-34, CD-99, Ki-67, and connective tissue growth factor/CCN2 in the fibrous region, S-100 in the adipose region, and Notch1 stain was observed in the eccrine sweat gland cells juxtaposed to the tumor adipose tissue, but no reactivity for Bcl-2, alphaSMA, Notch 2-4, CCN1, and CCN3.
  • Specific expression of CCN2 might be significant for the development of the tumor.
  • [MeSH-major] Fibroma / pathology. Head and Neck Neoplasms / metabolism. Head and Neck Neoplasms / pathology. Lipoma / pathology
  • [MeSH-minor] Adipose Tissue / chemistry. Adipose Tissue / pathology. Antigens, CD / analysis. Antigens, CD34 / analysis. Cell Adhesion Molecules / analysis. Connective Tissue Growth Factor. Humans. Immediate-Early Proteins / biosynthesis. Immunohistochemistry. Infant. Insulin-Like Growth Factor Binding Proteins / biosynthesis. Intercellular Signaling Peptides and Proteins / biosynthesis. Ki-67 Antigen / analysis. Male. Neoplasm Proteins / biosynthesis. Nephroblastoma Overexpressed Protein. Receptor, Notch1 / biosynthesis. S100 Proteins / analysis

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  • (PMID = 17466886.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / CD99 protein, human; 0 / CTGF protein, human; 0 / Cell Adhesion Molecules; 0 / Immediate-Early Proteins; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Ki-67 Antigen; 0 / NOTCH1 protein, human; 0 / NOV protein, human; 0 / Neoplasm Proteins; 0 / Nephroblastoma Overexpressed Protein; 0 / Receptor, Notch1; 0 / S100 Proteins; 139568-91-5 / Connective Tissue Growth Factor
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21. Kurita H, Kamata T, Koike T, Kobayashi H, Kurashina K: Intraoperative tissue staining of invaded oral carcinoma. Pathol Oncol Res; 2008 Dec;14(4):461-5
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  • [Title] Intraoperative tissue staining of invaded oral carcinoma.
  • The purpose of this study was to assess the ability of intraoperative tissue staining with consecutive application of 0.4% indigo carmine and 0.5% Congo red to demonstrate the extent and border of oral carcinoma invasion.
  • Once the oral tumor was resected, a vertical section of surgical specimen was taken from the central part of the tumor.
  • The extent and border of the invaded carcinoma were assessed on digital microscopic examination with tissue staining.
  • Tissue staining produced a brown-black stain on normal muscle, connective, and salivary tissues but not tumor and epithelial tissues.
  • It clearly demonstrated the extent and border of tumor invasion in 13 of 17 patients (76.5%); however, detection of remnant vital tumor cells in scar tissue after neoadjuvant chemotherapy, and distinction between the tumor and adipose tissue scattered in the muscle tissue was difficult.
  • The results of this study showed that intraoperative tissue staining was a possible method in demonstrating the extent and border of carcinoma deeply invaded in the soft tissue and selecting the site for additional frozen section analysis, although the method needed some refinement.
  • [MeSH-major] Carcinoma / pathology. Carcinoma / surgery. Mouth Neoplasms / pathology. Mouth Neoplasms / surgery. Neoplasm Staging / methods. Staining and Labeling / methods

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  • (PMID = 18575826.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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22. de Groot M, Appelman M, Spuls PI, de Rie MA, Bos JD: Initial experience with routine administration of etanercept in psoriasis. Br J Dermatol; 2006 Oct;155(4):808-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: We hypothesized: (i) that efficacy would be lower than that obtained in published phase II and III studies because (a) resistance to all conventional therapies as a reimbursement condition would select for more resistant cases and (b) inclusion would be more restricted to severe cases (higher PASI), and (ii) that efficacy would be lower in obese patients due to the possible role of adipose tissue in tumour necrosis factor (TNF)-alpha homeostasis.
  • Additionally, we related the clinical effect to the body mass index (BMI), for adipose tissue is thought to have a possible role in TNF-alpha homeostasis.
  • Although fatigue is not identified as a side-effect of etanercept, 10% of our patients reported fatigue as an adverse event during etanercept treatment.
  • Finally, the BMI does not seem to influence the patients' response to etanercept, although further investigations would be needed to confirm this.
  • [MeSH-major] Dermatologic Agents / therapeutic use. Immunoglobulin G / therapeutic use. Psoriasis / drug therapy. Receptors, Tumor Necrosis Factor / therapeutic use

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  • (PMID = 16965432.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dermatologic Agents; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; OP401G7OJC / Etanercept
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23. Cheng H, Dodge J, Mehl E, Liu S, Poulin N, van de Rijn M, Nielsen TO: Validation of immature adipogenic status and identification of prognostic biomarkers in myxoid liposarcoma using tissue microarrays. Hum Pathol; 2009 Sep;40(9):1244-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Validation of immature adipogenic status and identification of prognostic biomarkers in myxoid liposarcoma using tissue microarrays.
  • Expression profiling followed by tissue microarray validation linked to patient outcome is a powerful approach for validating biological mechanisms and identifying prognostic biomarkers.
  • We applied these techniques to independent series of primary myxoid liposarcomas in an effort to assess markers of adipose differentiation in myxoid liposarcoma and to identify prognostic markers that can be efficiently assessed by immunohistochemistry.
  • Candidate genes were selected based on analysis of expression profiles from 9 primary myxoid/round liposarcomas and 45 other soft tissue tumors, and by reference to publicly available data sets.
  • Protein products were validated on an adipose neoplasm tissue microarray, including 32 myxoid liposarcomas linked to patient outcome.
  • [MeSH-major] Adipogenesis. Biomarkers, Tumor / analysis. Liposarcoma, Myxoid / genetics. Soft Tissue Neoplasms / genetics. Tissue Array Analysis / methods

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  • (PMID = 19368956.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Insulin-Like Growth Factor Binding Protein 2; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Receptor, IGF Type 1
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24. Kuriu A, Shimono T, Kuwabara M, Ashikaga R, Hosono M, Murakami T: Fourth ventricular mixed germ cell tumor demonstrating adipose tissue in a young adult. Jpn J Radiol; 2010 Feb;28(2):166-8
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  • [Title] Fourth ventricular mixed germ cell tumor demonstrating adipose tissue in a young adult.
  • We report a case of fourth ventricular mixed germ cell tumor (GCT) in a 20-year-old man.
  • Neuroradiological investigations revealed a fourth ventricular hemorrhagic tumor with adipose tissue.
  • We suspected mixed GCT because adipose tissue was seen preoperatively, but mixed GCT occurring after childhood in this location has not previously been reported.
  • We describe herein the imaging findings for mixed GCT and discuss the differential diagnoses of fourth ventricular tumors with adipose tissue.
  • [MeSH-major] Adipose Tissue / pathology. Adipose Tissue / radiography. Brain Neoplasms / diagnosis. Fourth Ventricle / pathology. Fourth Ventricle / radiography. Neoplasms, Germ Cell and Embryonal / diagnosis
  • [MeSH-minor] Adult. Biomarkers / blood. Biomarkers, Tumor / blood. Cerebral Ventriculography / methods. Chorionic Gonadotropin / blood. Contrast Media. Diagnosis, Differential. Follow-Up Studies. Headache / etiology. Humans. Hydrocephalus / complications. Image Enhancement / methods. Magnetic Resonance Imaging / methods. Male. Tomography, X-Ray Computed / methods. Vomiting / etiology. Young Adult. alpha-Fetoproteins

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  • (PMID = 20182853.001).
  • [ISSN] 1867-108X
  • [Journal-full-title] Japanese journal of radiology
  • [ISO-abbreviation] Jpn J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin; 0 / Contrast Media; 0 / alpha-Fetoproteins
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25. McQueen C, Montgomery E, Dufour B, Olney MS, Illei PB: Giant hypopharyngeal atypical lipomatous tumor. Adv Anat Pathol; 2010 Jan;17(1):38-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Giant hypopharyngeal atypical lipomatous tumor.
  • Microscopically, they display an admixture of fibrovascular and adipose tissue that is coated by unremarkable squamous mucosa.
  • Here, we report a case that had scattered hyperchromatic cells and lipoblasts within the adipose tissue component.
  • In other anatomic sites similar appearing lesions have been interpreted as pedunculated liposarcomas/atypical lipomatous tumors that are more prone to local recurrences than classic giant fibrovascular polyps.
  • To confirm our suspicion of liposarcomatous differentiation, we performed immunohistochemistry for MDM2 and p53, 2 markers that are known to be negative in benign lipomatous lesions and positive in well-differentiated liposarcomas/atypical lipomatous tumors.
  • The scattered atypical hyperchromatic cells and the lipoblasts both exhibited strong nuclear staining for both markers and supported the diagnosis of pedunculated giant hypopharyngeal atypical lipomatous tumor.
  • [MeSH-major] Hypopharyngeal Neoplasms / pathology. Liposarcoma / pathology
  • [MeSH-minor] Humans. Immunohistochemistry. Male. Middle Aged. Polyps / diagnosis. Proto-Oncogene Proteins c-mdm2 / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 20032637.001).
  • [ISSN] 1533-4031
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Number-of-references] 51
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26. Scariot R, Giovanini AF, Torres-Pereira CC, Piazzetta CM, Costa DJ, Rebellato NL, Müller PR: Massive growth of an intraoral lipoma. J Contemp Dent Pract; 2008;9(7):115-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Lipoma, a benign tumor of adipose tissue, is rarely seen in the oral cavity.
  • A clinical diagnosis of lipoma was established, and the treatment consisted of complete excision of the mass under local anesthesia.
  • [MeSH-major] Cheek / pathology. Lipoma / pathology. Mouth Neoplasms / pathology

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  • (PMID = 18997924.001).
  • [ISSN] 1526-3711
  • [Journal-full-title] The journal of contemporary dental practice
  • [ISO-abbreviation] J Contemp Dent Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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27. Vicioso L, Gallego E, Sanz A: Cutaneous mixed tumor with lipomatous stroma. J Cutan Pathol; 2006 Sep;33 Suppl 2:35-8
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  • [Title] Cutaneous mixed tumor with lipomatous stroma.
  • AIM: Mixed tumors are usually composed of two components, one epithelial and the other mesenchymal.
  • The latter component is commonly myxoid or myxochondroid; a massively lipomatous stroma is very unusual.
  • To date, only two cases of mixed tumor of the skin have been reported with this type of stroma.
  • METHODS AND RESULTS: We report the case of a 61-year-old man with a mixed tumor situated on the hand, an unusual site for these tumors, with over 90% of the tumor composed of adipose tissue.
  • The tumor was a well-circumscribed, 4.5-cm mass, with the gross appearance of a lipoma.
  • The lipomatous stroma contained nests and ribbons of epithelial cells, with occasional tubular structures, surrounded by a scarce amount of fibromyxoid tissue.
  • Immunohistochemical study showed findings similar to those seen in classic mixed tumors.
  • CONCLUSION: Together with a few other cases in the skin and parotid gland, this report shows how massive adipose differentiation can arise in a mixed tumor of the skin.
  • [MeSH-major] Adipose Tissue / pathology. Fibroma / pathology. Mixed Tumor, Malignant / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 16972952.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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28. Barazzoni R, Biolo G, Zanetti M, Bernardi A, Guarnieri G: Inflammation and adipose tissue in uremia. J Ren Nutr; 2006 Jul;16(3):204-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammation and adipose tissue in uremia.
  • Adipose tissue produces several hormones (adipocytokines including leptin, resistin, tumor necrosis factor-alpha, and adiponectin) that modulate both systemic inflammatory response and insulin action.
  • High leptin, resistin, and tumor necrosis factor-alpha and low adiponectin are associated with proinflammatory conditions, whereas opposite patterns are commonly observed in the presence of increased insulin sensitivity, low inflammation, and reduced cardiovascular risk.
  • The potential role of altered adipose tissue adipocytokine production in the onset of renal failure-associated inflammatory and metabolic derangements remains largely to be elucidated and is discussed in the current report.
  • [MeSH-major] Adipose Tissue. Inflammation. Uremia

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  • (PMID = 16825020.001).
  • [ISSN] 1532-8503
  • [Journal-full-title] Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation
  • [ISO-abbreviation] J Ren Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Cytokines; 0 / Ghrelin; 0 / Leptin; 0 / Peptide Hormones
  • [Number-of-references] 34
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29. Bulcão C, Ferreira SR, Giuffrida FM, Ribeiro-Filho FF: The new adipose tissue and adipocytokines. Curr Diabetes Rev; 2006 Feb;2(1):19-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The new adipose tissue and adipocytokines.
  • Obesity is a well-known risk factor for the development of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease.
  • Rather than the total amount of fat, central distribution of adipose tissue is very important in the pathophysiology of this constellation of abnormalities termed metabolic syndrome.
  • Adipose tissue, regarded only as an energy storage organ until the last decade, is now known as the biggest endocrine organ of the human body.
  • This tissue secretes a number of substances--adipocytokines--with multiple functions in metabolic profile and immunological process.
  • In this review we discuss visceral obesity, the potential mechanisms by which it would be related to insulin resistance, methods for its assessment and focus on the main adipocytokines expressed and secreted by the adipose tissue.
  • [MeSH-major] Adipokines / physiology. Adipose Tissue / physiology. Obesity / physiopathology
  • [MeSH-minor] Abdomen. Adiponectin / physiology. Humans. Interleukin-6 / physiology. Leptin / physiology. Plasminogen Activator Inhibitor 1 / physiology. Resistin / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 18220614.001).
  • [ISSN] 1573-3998
  • [Journal-full-title] Current diabetes reviews
  • [ISO-abbreviation] Curr Diabetes Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Adipokines; 0 / Adiponectin; 0 / Interleukin-6; 0 / Leptin; 0 / Plasminogen Activator Inhibitor 1; 0 / Resistin; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 196
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30. Hemmrich K, von Heimburg D: Biomaterials for adipose tissue engineering. Expert Rev Med Devices; 2006 Sep;3(5):635-45
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  • [Title] Biomaterials for adipose tissue engineering.
  • There is high clinical need for an adequate reconstruction of soft tissue defects as found after tumor resections, deep burns or severe trauma.
  • A promising solution for these defects is adipose tissue engineering, with adult stem cells of the adipose tissue, implanted on 3D biomaterials.
  • They can be yielded from excised adipose tissue or liposuction material.
  • When preadipocytes are seeded on carriers for the generation of adipose tissue, chemical composition, mechanical stability and 3D architecture of the construct are crucial factors.
  • They ensure cellular penetration into the construct, sufficient proliferation on the material and full differentiation inside the construct after transplantation.
  • Over recent years, in vivo trials in particular have allowed significant insights into the potential, the perspectives, but also the current difficulties and draw-backs in adipose tissue engineering.
  • This review focuses on the main strategies in adipose tissue regeneration, compares the various materials that have been used as carrier matrices so far and considers them in light of the challenges they have yet to meet.
  • [MeSH-major] Adipocytes / cytology. Adipose Tissue. Biocompatible Materials / chemistry. Stem Cells / cytology. Tissue Engineering / methods
  • [MeSH-minor] Animals. Biopolymers / chemistry. Cell Differentiation. Humans. Hydrogels / chemistry

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  • (PMID = 17064248.001).
  • [ISSN] 1743-4440
  • [Journal-full-title] Expert review of medical devices
  • [ISO-abbreviation] Expert Rev Med Devices
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biocompatible Materials; 0 / Biopolymers; 0 / Hydrogels
  • [Number-of-references] 72
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31. Spinelli C, Costanzo S, Severi E, Giannotti G, Massart F: A thoracic wall lipoblastoma in a 3-month-old infant: A case report and review of the literature. J Pediatr Hematol Oncol; 2006 Sep;28(9):594-600

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  • Lipoblastoma is a rare benign tumor of adipose tissue seen almost always in infancy and early childhood.
  • Lipoblastoma is a tumor with good prognosis with no reported metastases, despite its potential for local invasion and rapid growth.
  • With the aim of both diagnosis and treatment, the lipomatous mass was removed by local resection.
  • In addition to the patient's age, histologic and cytogenetic analyses assisted the diagnosis of diffuse lipoblastoma.
  • [MeSH-major] Lipoma / genetics. Lipoma / pathology. Soft Tissue Neoplasms / genetics. Soft Tissue Neoplasms / pathology. Thoracic Wall / pathology

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  • (PMID = 17006266.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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32. He M, Aisner S, Benevenia J, Patterson F, Aviv H, Hameed M: p16 immunohistochemistry as an alternative marker to distinguish atypical lipomatous tumor from deep-seated lipoma. Appl Immunohistochem Mol Morphol; 2009 Jan;17(1):51-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p16 immunohistochemistry as an alternative marker to distinguish atypical lipomatous tumor from deep-seated lipoma.
  • Atypical lipomatous tumor (ALT)/well-differentiated liposarcoma (WDLPS) is a locally aggressive malignant mesenchymal neoplasm, resembling ordinary lipoma in many clinical aspects.
  • Fifty cases of lipomatous neoplasms, with cytogenetic results, from 45 patients were collected from the archives in Department of Pathology, University of Medicine and Dentistry of New Jersey/New Jersey Medical School during 1998 to 2006.

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  • (PMID = 18779733.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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33. Berstein LM: [Hormones of adipose tissue (adipocytokines): ontogenetic and oncologic aspects]. Adv Gerontol; 2005;16:51-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hormones of adipose tissue (adipocytokines): ontogenetic and oncologic aspects].
  • Being an important component of body composition, adipose tissue accepts a lot of hormonal signals and, besides, is able to produce hormone-like peptides, named adipokines or adipocytokines, and participate in the metabolism of steroid hormones.
  • Endocrine properties of adipose tissue are dependent of its volume, morphology (size and number of adipocytes), fat topography (visceral and subcutaneous fat), characteristics of distinct fat depot (including mammary fat), some features of genome, etc.
  • Certain characteristics of the adipose organ are formed and then realized in pre- and postnatal life (pregnancy and fetal programming), in duration of puberty, after menopause and with aging.
  • Adipocyte and non-adipocyte compartments of adipose tissue are involved into reactions of immunity/inflammation and into development of glucose intolerance and insulin resistance.
  • The balance among adipocytokines (adipocytokine net or lattice) with distinct properties (TNF-alpha, leptin and adiponectin as an examples) and between adipocytokines and steroid-producing capacity of adipose tissue is an important variable representing a basis for the modification of cardiovascular and oncological morbidity risk as well as a target for geroprotection and cancer prevention.

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  • (PMID = 16075677.001).
  • [ISSN] 1561-9125
  • [Journal-full-title] Advances in gerontology = Uspekhi gerontologii
  • [ISO-abbreviation] Adv Gerontol
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Cytokines; 0 / Intercellular Signaling Peptides and Proteins; 0 / Leptin; 0 / Peptide Hormones; 0 / Steroids; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 87
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34. Okada S, Kozuka C, Masuzaki H, Yasue S, Ishii-Yonemoto T, Tanaka T, Yamamoto Y, Noguchi M, Kusakabe T, Tomita T, Fujikura J, Ebihara K, Hosoda K, Sakaue H, Kobori H, Ham M, Lee YS, Kim JB, Saito Y, Nakao K: Adipose tissue-specific dysregulation of angiotensinogen by oxidative stress in obesity. Metabolism; 2010 Sep;59(9):1241-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose tissue-specific dysregulation of angiotensinogen by oxidative stress in obesity.
  • Adipose tissue expresses all components of the renin-angiotensin system including angiotensinogen (AGT).
  • Recent studies have highlighted a potential role of AGT in adipose tissue function and homeostasis.
  • However, some controversies surround the regulatory mechanisms of AGT in obese adipose tissue.
  • In this context, we here demonstrated that the AGT messenger RNA (mRNA) level in human subcutaneous adipose tissue was significantly reduced in obese subjects as compared with nonobese subjects.
  • Adipose tissue AGT mRNA level in obese mice was also lower as compared with their lean littermates; however, the hepatic AGT mRNA level remained unchanged.
  • Treatment of the 3T3-L1 and primary adipocytes with reactive oxygen species (hydrogen peroxide) or tumor necrosis factor alpha caused a significant decrease in the expression and secretion of AGT.
  • Finally, treatment of obese db/db mice with N-acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver.
  • The present study demonstrates for the first time that oxidative stress dysregulates AGT in obese adipose tissue, providing a novel insight into the adipose tissue-specific interaction between the regulation of AGT and oxidative stress in the pathophysiology of obesity.
  • [MeSH-minor] Adult. Animals. Cell Size. Cells, Cultured. Female. Humans. Male. Mice. Mice, Obese. Middle Aged. Oxidative Stress. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20045538.001).
  • [ISSN] 1532-8600
  • [Journal-full-title] Metabolism: clinical and experimental
  • [ISO-abbreviation] Metab. Clin. Exp.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK072408; United States / NIDDK NIH HHS / DK / R01 DK072408-01A1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 11002-13-4 / Angiotensinogen
  • [Other-IDs] NLM/ NIHMS169981; NLM/ PMC2891233
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35. Walter M, Liang S, Ghosh S, Hornsby PJ, Li R: Interleukin 6 secreted from adipose stromal cells promotes migration and invasion of breast cancer cells. Oncogene; 2009 Jul 30;28(30):2745-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin 6 secreted from adipose stromal cells promotes migration and invasion of breast cancer cells.
  • Although adipose tissue-derived estrogen contributes to obesity-associated risk for estrogen receptor (ER)-positive breast cancer, the estrogen-independent impact of adipose tissue on tumor invasion and progression needs to be elucidated.
  • Here, we show that adipose stromal cells (ASCs) significantly stimulate migration and invasion of ER-negative breast cancer cells in vitro and tumor invasion in a co-transplant xenograft mouse model.
  • Our study also identifies cofilin-1, a known regulator of actin dynamics, as a determinant of the tumor-promoting activity of ASCs.
  • Depletion of IL-6 from the ASC-conditioned medium abrogated the stimulatory effect of ASCs on the migration and invasion of breast tumor cells.

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  • (PMID = 19483720.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA093506-08; United States / NCI NIH HHS / CA / R01 CA093506; United States / NCI NIH HHS / CA / R01 CA093506-05A1; United States / NCI NIH HHS / CA / CA093506-05A1; United States / NCI NIH HHS / CA / CA93506; United States / NCI NIH HHS / CA / CA093506-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cofilin 1; 0 / Interleukin-6; 0 / ROCK1 protein, human; EC 2.7.11.1 / rho-Associated Kinases
  • [Other-IDs] NLM/ NIHMS111638; NLM/ PMC2806057
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36. Dahlman I, Arner P: Obesity and polymorphisms in genes regulating human adipose tissue. Int J Obes (Lond); 2007 Nov;31(11):1629-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Obesity and polymorphisms in genes regulating human adipose tissue.
  • Adipose tissue contains the largest store of energy in the body and plays important roles in regulating energy partitioning.
  • Developments in genomics, in particular microarray-based expression profiling, have provided scientists with a number of new candidate genes whose expression in adipose tissue is regulated by obesity.
  • This article provides a comprehensive review of adipose-tissue-expressed genes implicated in predisposition to human obesity.
  • The authors consider the following genes of particular interest: peroxisome proliferator-activated receptor gamma and, potentially, INSIG2 acting in adipogenesis; the adrenoreceptors beta 2 and 3, as well as hormone-sensitive lipase acting on lipolysis; uncoupling protein 2 acting in mitochondria energy expenditure; and among secreted molecules the cytokine tumor necrosis factor alpha and the hormone leptin.
  • With the rapid development in genome research, we predict that additional alleles in genes regulating adipose tissue function will be established as risk factors for common obesity in the coming years.
  • [MeSH-major] Adipose Tissue / metabolism. Obesity / genetics. Polymorphism, Genetic
  • [MeSH-minor] Adipocytes / physiology. Adipogenesis / genetics. Gene Expression Profiling / methods. Gene Expression Regulation. Genetic Predisposition to Disease. Humans. Insulin / physiology. Lipolysis / genetics. Mitochondria / physiology

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  • (PMID = 17563763.001).
  • [ISSN] 0307-0565
  • [Journal-full-title] International journal of obesity (2005)
  • [ISO-abbreviation] Int J Obes (Lond)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin
  • [Number-of-references] 190
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37. Maury E, Brichard SM: Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome. Mol Cell Endocrinol; 2010 Jan 15;314(1):1-16
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome.
  • This dysregulation of adipokine production may promote obesity-linked metabolic disorders and cardiovascular disease.
  • Besides considering adipokines, this review will also highlight the cellular key players and molecular mechanisms involved in adipose inflammation.
  • Targeting the changes in the cellular composition of adipose tissue, the underlying molecular mechanisms, and the altered production of adipokines may have therapeutic potential in the management of the metabolic syndrome.
  • [MeSH-major] Adipokines / immunology. Adipose Tissue. Inflammation / immunology. Metabolic Syndrome X
  • [MeSH-minor] Adipocytes / cytology. Adipocytes / metabolism. Adiponectin / metabolism. Body Fat Distribution. Chemokines / immunology. Cytokines / immunology. Cytokines / metabolism. Humans. Insulin / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Macrophages / cytology. Macrophages / immunology. Nicotinamide Phosphoribosyltransferase / metabolism. Obesity / metabolism. Signal Transduction / physiology. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 19682539.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / APLN protein, human; 0 / Adipokines; 0 / Adiponectin; 0 / Chemokines; 0 / Cytokines; 0 / Insulin; 0 / Intercellular Signaling Peptides and Proteins; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
  • [Number-of-references] 232
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38. Cates JM, Coffing BN, Harris BT, Black CC: Calretinin expression in tumors of adipose tissue. Hum Pathol; 2006 Mar;37(3):312-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calretinin expression in tumors of adipose tissue.
  • Although well established as a marker of mesothelial cells, calretinin is also expressed in several other tissue types, including adipose tissue.
  • Accordingly, immunohistochemical staining for calretinin has been described in an increasing number of neoplasms other than mesothelioma.
  • A detailed analysis of calretinin expression in lipogenic tumors has not yet been reported, however.
  • Given the known expression patterns of calretinin in normal tissues, we predicted that calretinin immunoreactivity would be detected in lipoma and the various histologic subtypes of liposarcoma, and that this marker might be of use in the differential diagnosis of selected fatty tumors.
  • Calretinin immunoreactivity was detected, at least focally, in all 10 samples of normal adipose tissue and in 22 of 23 lipomas or lipoma variants.
  • Pleomorphic variants of other sarcomas, including undifferentiated high-grade pleomorphic sarcoma, rhabdomyosarcoma, leiomyosarcoma, and malignant peripheral nerve sheath tumor also exhibited focal calretinin immunoreactivity in a minority of cases, as did some small round cell sarcomas.
  • These results suggest that calretinin immunoreactivity in normal and neoplastic adipose tissue is more ubiquitous than previously reported and may be a useful, albeit nonspecific marker of lipogenic differentiation.
  • However, its utility in the differential diagnosis of fatty tumors appears limited.
  • [MeSH-major] Adipose Tissue / metabolism. Lipoma / metabolism. Liposarcoma / metabolism. S100 Calcium Binding Protein G / metabolism. Soft Tissue Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Calbindin 2. Humans. Immunoenzyme Techniques. Retrospective Studies. Tissue Array Analysis

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  • (PMID = 16613326.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / S100 Calcium Binding Protein G
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39. Sopasakis VR, Nagaev I, Smith U: Cytokine release from adipose tissue of nonobese individuals. Int J Obes (Lond); 2005 Sep;29(9):1144-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokine release from adipose tissue of nonobese individuals.
  • Explants of human adipose tissue from nonobese subjects were cultured for 24 h with or without the presence of 20 ng/ml TNFalpha.
  • TNFalpha increased the mRNA levels of TNFalpha itself as well as IL-6, IL-8, IL-1beta and PAI-1, but not leptin.
  • Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha.
  • However, since neither TNFalpha, resistin or IL-1beta was found in the culture medium, such a regulatory effect by TNFalpha on adipose tissue in vivo is likely to be mediated through a paracrine mechanism where invaded inflammatory cells may play a critical role.
  • [MeSH-major] Adipose Tissue / metabolism. Cytokines / analysis
  • [MeSH-minor] Female. Gene Expression Regulation. Humans. Interleukin-1 / analysis. Interleukin-6 / analysis. Interleukin-8 / analysis. Leptin / analysis. Male. Middle Aged. Plasminogen Activator Inhibitor 1 / analysis. RNA, Messenger / analysis. Receptors, Interleukin-1 / antagonists & inhibitors. Resistin / analysis. Tissue Culture Techniques / methods. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 15917841.001).
  • [ISSN] 0307-0565
  • [Journal-full-title] International journal of obesity (2005)
  • [ISO-abbreviation] Int J Obes (Lond)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Leptin; 0 / Plasminogen Activator Inhibitor 1; 0 / RNA, Messenger; 0 / Receptors, Interleukin-1; 0 / Resistin; 0 / Tumor Necrosis Factor-alpha
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40. Prantl L, Muehlberg F, Navone NM, Song YH, Vykoukal J, Logothetis CJ, Alt EU: Adipose tissue-derived stem cells promote prostate tumor growth. Prostate; 2010 Nov 1;70(15):1709-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose tissue-derived stem cells promote prostate tumor growth.
  • BACKGROUND: Recent evidence indicates that cancer stem cells play an important role in tumor initiation and maintenance.
  • Additionally, the effect of tissue-resident stem cells located in the surrounding healthy tissue on tumor progression has been demonstrated.
  • While most knowledge has been derived from studies of breast cancer cells, little is known regarding the influence of tissue resident stem cells on the tumor biology of prostate cancer.
  • (1) subcutaneous injection of 10(6) MDA PCa 118b human prostate cancer cells into the upper back or (2) subcutaneous injection of 10(6) MDA PCa 118b cells mixed directly with 10(5) GFP-labeled human adipose tissue-derived stem cells (hASCs).
  • Tumor growth and volumes over the ensuing 3 weeks were assessed using calipers and micro-computed tomography.
  • Immunohistochemistry was performed to identify engrafted hASCs in tumor sections.
  • RESULTS: At 3 weeks after injection, the mean tumor volume in the MDA PCa 118b/hASC co-injection group (1019.95 ± 73.49 mm(3)) was significantly higher than that in the MDA PCa 118b-only group (308.70 ± 21.06 mm(3)).
  • Engrafted hASCs exhibited the nuclear marker of proliferation Ki67 and expressed markers for endothelial differentiation, indicating their engraftment in tumor vessels.
  • CONCLUSION: Our study revealed for the first time that ASCs subcutaneously co-injected with prostate cancer cells engraft and promote tumor progression.
  • Further evaluation of the cross-talk between tumor and local tissue-resident stem cells may lead to new strategies for prostate cancer therapy.
  • [MeSH-major] Adipose Tissue / cytology. Neoplastic Stem Cells / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Disease Models, Animal. Flow Cytometry. Immunophenotyping. Male. Mice. Mice, Nude. Neoplasm Transplantation / methods. Random Allocation. Tomography, X-Ray Computed

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  • (PMID = 20564322.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS612155; NLM/ PMC4977846
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41. Pi-Sunyer FX: The relation of adipose tissue to cardiometabolic risk. Clin Cornerstone; 2006;8 Suppl 4:S14-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The relation of adipose tissue to cardiometabolic risk.
  • Adipose tissue is an active and complex endocrine organ that secretes numerous bioactive substances, including hormones, growth factors, and cytokines.
  • Central obesity, one of the components of metabolic syndrome, is a cardiometabolic risk factor associated with a state of chronic inflammation and coagulation, one in which the expression of certain adipocytokines, including tumor necrosis factor-alpha (TNF-(alpha), interleukin (IL)-6, and plasminogen activator inhibitor-1 (PAI-1) is more abundantly increased, while adiponectin expression is decreased.
  • TNF-alpha initiates and organizes inflammatory changes in vascular tissue.
  • IL-6, an inflammatory cytokine directly implicated in atherogenesis, exerts pleiotropic effects on a variety of tissues.
  • Weight loss has long been promoted as a means to reduce the risk of type 2 diabetes and cardiovascular disease; for example, exercise and a hypocaloric diet have been shown to decrease PAI-1 levels.
  • These agents may play a role in the regulation of adipocytokines, which may directly affect the risk for cardiometabolic disease.
  • [MeSH-major] Adiponectin / metabolism. Adipose Tissue / metabolism. Atherosclerosis / metabolism. Cytokines / metabolism

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  • (PMID = 17208662.001).
  • [ISSN] 1098-3597
  • [Journal-full-title] Clinical cornerstone
  • [ISO-abbreviation] Clin Cornerstone
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Cytokines
  • [Number-of-references] 53
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42. Birk RZ, Rubinstein M: IFN-alpha induces apoptosis of adipose tissue cells. Biochem Biophys Res Commun; 2006 Jun 30;345(2):669-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IFN-alpha induces apoptosis of adipose tissue cells.
  • Interferon alpha (IFN-alpha) is produced in response to viral infections and used clinically in the therapy of a variety of cancers and viral infections.
  • The body weight and adipose cell size of IFN-alpha A/D-treated DIO mice were significantly lower (P<0.05 and P<0.001, respectively) as compared with those of control DIO mice.
  • PI3K and Bcl-2 were down-regulated whereas Bax expression was elevated in adipose tissue following IFN treatment as compared to adipose tissue of control DIO mice.
  • [MeSH-major] Adipocytes / drug effects. Adipose Tissue / drug effects. Apoptosis / drug effects. Body Weight / drug effects. Interferon-alpha / pharmacology
  • [MeSH-minor] 3T3-L1 Cells. Animals. Antineoplastic Agents / pharmacology. Down-Regulation. Humans. Mice. Mice, Inbred C57BL. Obesity / drug therapy. Obesity / pathology. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Time Factors. Tumor Cells, Cultured. bcl-2-Associated X Protein / metabolism

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  • (PMID = 16696938.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / Pik3cd protein, mouse
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43. Takaoka M, Suzuki H, Shioda S, Sekikawa K, Saito Y, Nagai R, Sata M: Endovascular injury induces rapid phenotypic changes in perivascular adipose tissue. Arterioscler Thromb Vasc Biol; 2010 Aug;30(8):1576-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endovascular injury induces rapid phenotypic changes in perivascular adipose tissue.
  • OBJECTIVE: Accumulating evidence suggests that adipose tissue not only stores energy but also secretes various bioactive substances called adipocytokines.
  • METHODS AND RESULTS: Endovascular injury significantly upregulated proinflammatory adipocytokines and downregulated adiponectin within periadventitial fat tissue in models of mouse femoral artery wire injury and rat iliac artery balloon injury.
  • Genetic disruption of tumor necrosis factor (TNF)-alpha attenuated upregulation of proinflammatory adipocytokine expression, with reduced neointimal hyperplasia after vascular injury.
  • CONCLUSIONS: Our findings indicate that endovascular injury induces rapid and marked changes in perivascular adipose tissue, mainly mediated by TNF-alpha.
  • It is suggested that the phenotypic changes in perivascular adipose tissue may have a role in the pathogenesis of neointimal hyperplasia after angioplasty.
  • [MeSH-major] Adipose Tissue / pathology. Carotid Artery Injuries / pathology
  • [MeSH-minor] 3T3-L1 Cells. Adipokines / metabolism. Angioplasty, Balloon / adverse effects. Animals. Cell Proliferation. Chemokine CCL2 / deficiency. Chemokine CCL2 / genetics. Coculture Techniques. Culture Media, Conditioned / metabolism. Disease Models, Animal. Hyperplasia. Inflammation Mediators / metabolism. Interleukin-6 / deficiency. Interleukin-6 / genetics. Macrophages / immunology. Macrophages / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Muscle, Smooth, Vascular / immunology. Muscle, Smooth, Vascular / pathology. Myocytes, Smooth Muscle / immunology. Myocytes, Smooth Muscle / pathology. Phenotype. Rats. Rats, Wistar. Time Factors. Tumor Necrosis Factor-alpha / deficiency. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 20489168.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / Culture Media, Conditioned; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
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44. Gambero A, Maróstica M, Abdalla Saad MJ, Pedrazzoli J Jr: Mesenteric adipose tissue alterations resulting from experimental reactivated colitis. Inflamm Bowel Dis; 2007 Nov;13(11):1357-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mesenteric adipose tissue alterations resulting from experimental reactivated colitis.
  • BACKGROUND: Adipose tissue secretes a large number of hormones that act either locally or at distant sites, modulating immune responses, inflammation, and many endocrine and metabolic functions.
  • Abnormalities of fat in the mesentery have been long recognized in surgical specimens as characteristic features of Crohn's disease; however, the importance of this in chronic inflammatory disease is unknown.
  • Additionally, adipocytes in depots that enclose lymph nodes or other dense masses of lymphoid tissue have many site-specific physiological properties.
  • METHODS: In this study, the alterations of mesenteric and perinodal mesenteric adipose tissue during experimental colitis, induced by repeated intracolonic trinitrobenzene sulfonic acid instillations, were evaluated, focusing on morphological and activity alterations and the adipocytokine production profile.
  • Another adipose tissue depot, epididymal adipose tissue, was also evaluated and no change in mass was observed.
  • CONCLUSIONS: The findings suggest that mesenteric adipose tissue has a site-specific response during experimental inflammation, where perinodal adipose tissue retains the ability to produce different adipocytokines.
  • These substances may interfere in many lymph node aspects, while mesenteric adipose tissue produces substances that could contribute directly to aggravate the inflammatory process.
  • [MeSH-major] Adipose Tissue / pathology. Colitis / pathology. Mesentery / pathology
  • [MeSH-minor] Adipokines / biosynthesis. Animals. Crohn Disease. Disease Models, Animal. Lipolysis. Lymph Nodes / pathology. PPAR gamma. Rats. Tumor Necrosis Factor-alpha

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  • (PMID = 17604368.001).
  • [ISSN] 1078-0998
  • [Journal-full-title] Inflammatory bowel diseases
  • [ISO-abbreviation] Inflamm. Bowel Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / PPAR gamma; 0 / Tumor Necrosis Factor-alpha
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45. Jotzu C, Alt E, Welte G, Li J, Hennessy BT, Devarajan E, Krishnappa S, Pinilla S, Droll L, Song YH: Adipose tissue-derived stem cells differentiate into carcinoma-associated fibroblast-like cells under the influence of tumor-derived factors. Anal Cell Pathol (Amst); 2010;33(2):61-79
MedlinePlus Health Information. consumer health - Stem Cells.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose tissue-derived stem cells differentiate into carcinoma-associated fibroblast-like cells under the influence of tumor-derived factors.
  • Carcinoma-associated fibroblasts (CAF) are considered to contribute to tumor growth, invasion and metastasis.
  • Since human adipose tissue-derived stem cells (hASCs) are locally adjacent to breast cancer cells and might directly interact with tumor cells, we investigated whether CAFs may originate from hASCs.
  • The conditioned medium from MDAMB231 and MCF7 contains significant amounts of transforming growth factor-beta 1 (TGFβ1) and the differentiation of hASCs towards CAFs is dependent on TGFβ1 signaling via Smad3 in hASCs.
  • Additionally, we found that these hASC-derived CAF-like cells exhibit functional properties of CAFs, including the ability to promote tumor cell invasion in an in vitro invasion assay, as well as increased expression of stromal-cell-derived factor 1 (SDF-1) and CCL5.
  • Taken together, these data suggest that hASCs are a source of CAFs which play an important role in the tumor invasion.
  • [MeSH-major] Adipocytes / cytology. Cell Differentiation. Fibroblasts / cytology. Neoplasms / pathology. Stem Cells / cytology
  • [MeSH-minor] Cell Line, Tumor. Humans. Signal Transduction

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  • (PMID = 20978328.001).
  • [ISSN] 2210-7185
  • [Journal-full-title] Analytical cellular pathology (Amsterdam)
  • [ISO-abbreviation] Anal Cell Pathol (Amst)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC4605656
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46. Walker GE, Verti B, Marzullo P, Savia G, Mencarelli M, Zurleni F, Liuzzi A, Di Blasio AM: Deep subcutaneous adipose tissue: a distinct abdominal adipose depot. Obesity (Silver Spring); 2007 Aug;15(8):1933-43
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  • [Title] Deep subcutaneous adipose tissue: a distinct abdominal adipose depot.
  • OBJECTIVE: Abdominal visceral (VAT) and subcutaneous adipose tissue (SAT) display significant metabolic differences, with VAT showing a functional association to metabolic/cardiovascular disorders.
  • A third abdominal adipose layer, derived by the division of SAT and identified as deep subcutaneous adipose tissue (dSAT), may play a significant and independent metabolic role.
  • Samples were evaluated for depot-specific differences in insulin sensitivity using adiponectin, glucose transport protein 4 (GLUT4), and resistin mRNA and protein expression, glucocorticoid metabolism by 11beta-hydroxysteroid dehydrogenase type-1 (11beta-HSD1) expression, and alterations in the adipokines leptin and tumor necrosis factor-alpha (TNF-alpha).
  • DISCUSSION: Overall, dSAT seems to be a distinct abdominal adipose depot supporting an independent metabolic function that may have a potential role in the development of obesity-associated complications.
  • [MeSH-minor] 11-beta-Hydroxysteroid Dehydrogenase Type 1 / biosynthesis. 11-beta-Hydroxysteroid Dehydrogenase Type 1 / genetics. 11-beta-Hydroxysteroid Dehydrogenase Type 1 / metabolism. Adipocytes / metabolism. Adiponectin / biosynthesis. Adiponectin / genetics. Adiponectin / metabolism. Blotting, Western. Female. Glucocorticoids / metabolism. Glucose / metabolism. Glucose Transporter Type 4 / biosynthesis. Glucose Transporter Type 4 / genetics. Glucose Transporter Type 4 / metabolism. Humans. Hypoxanthine Phosphoribosyltransferase / biosynthesis. Hypoxanthine Phosphoribosyltransferase / genetics. Hypoxanthine Phosphoribosyltransferase / metabolism. Leptin / genetics. Leptin / metabolism. Male. Middle Aged. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Vascular Endothelial Growth Factor / biosynthesis. Receptors, Vascular Endothelial Growth Factor / genetics. Receptors, Vascular Endothelial Growth Factor / metabolism. Resistin / biosynthesis. Resistin / genetics. Resistin / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17712110.001).
  • [ISSN] 1930-7381
  • [Journal-full-title] Obesity (Silver Spring, Md.)
  • [ISO-abbreviation] Obesity (Silver Spring)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Glucocorticoids; 0 / Glucose Transporter Type 4; 0 / Leptin; 0 / RETN protein, human; 0 / RNA, Messenger; 0 / Resistin; 0 / SLC2A4 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 1; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; IY9XDZ35W2 / Glucose
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47. Pandzić Jaksić V: [Adipocytokines as mediators of metabolic role of adipose tissue]. Acta Med Croatica; 2010 Oct;64(4):253-62
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  • [Title] [Adipocytokines as mediators of metabolic role of adipose tissue].
  • The discovery of adipocytokines, products of adipose tissue, has been a turning point in the understanding of metabolic disorders.
  • Historically considered as a passive depot of energy, adipose tissue has become an important active participant and adipocytokines crucial mediators of its metabolic role.
  • Among a number of adipose tissue products, leptin and adiponectin are exclusively secreted by adipocytes.
  • Recent investigations have also emphasized the important role of resistin, visfatin, retinol binding protein 4, and of a whole list of cytokines like interleukin-6, tumor necrosis factor a, plasminogen activator inhibitor-1, or a chemokine, monocyte chemoattractant protein-1.
  • The fact that secretory balance of adipose tissue in obesity is shifted towards the proinflammatory spectrum has supported the hypothesis on the development of dysfunctional adipose tissue in these circumstances.
  • [MeSH-major] Adipokines / physiology. Adipose Tissue / metabolism

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  • (PMID = 21688608.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Adipokines
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48. Yamaguchi T, Takimoto T, Yamashita T, Kitahara S, Omura M, Ueda Y: Fat-containing variant of solitary fibrous tumor (lipomatous hemangiopericytoma) arising on surface of kidney. Urology; 2005 Jan;65(1):175
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  • [Title] Fat-containing variant of solitary fibrous tumor (lipomatous hemangiopericytoma) arising on surface of kidney.
  • Fat-containing variant of a solitary fibrous tumor is a recently recognized benign soft-tissue tumor that usually affects the thigh and retroperitoneum.
  • We report a 51-year-old woman with a fat-containing variant of a solitary fibrous tumor that is the first reported case involving a visceral organ.
  • The tumor was well delineated and seemed to arise from the renal capsule, radiographically and macroscopically.
  • The tumor microscopically mimicked a solitary fibrous tumor but exhibited focal aggregates of fat cells.
  • A fat-containing variant of a solitary fibrous tumor involving the kidney should be distinguished from spindle cell carcinoma, angiomyolipoma, gastrointestinal stromal tumor, and cellular schwannoma.
  • [MeSH-major] Adipose Tissue / pathology. Hemangiopericytoma / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Female. Humans. Middle Aged. Nephrectomy. Tomography, X-Ray Computed

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  • (PMID = 15667897.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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49. Matsuzawa Y: White adipose tissue and cardiovascular disease. Best Pract Res Clin Endocrinol Metab; 2005 Dec;19(4):637-47

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] White adipose tissue and cardiovascular disease.
  • Tumour necrosis factor (TNF)-alphaalpha, plasminogen activator inhibitor-1 (PAI-1) and heparin-binding epidermal-growth-factor-like growth factor (HBEGF) are among these adipocytokines, and they contribute to the development of vascular diseases.
  • Visfatin is a visceral fat-specific protein that may be related to the development of obesity-related diseases such as diabetes mellitus and cardiovascular disease.
  • In contrast, adiponectin, an adipose-tissue-specific collagen-like protein, has recently been reported as an important anti-atherogenic and anti-diabetic protein.
  • Visceral fat accumulation leads to dysfunction of adipocytes (including hypersecretion of TNF-alphaalpha, PAI-1 and HBEGF, and hyposecretion of adiponectin), which results in the development of a variety of metabolic and circulatory diseases.
  • In this review, the importance of adipocytokines, including adiponectin, is discussed with respect to cardiovascular disease.
  • [MeSH-major] Adipose Tissue / physiology. Cardiovascular Diseases / physiopathology
  • [MeSH-minor] Adipocytes / physiology. Adiponectin / physiology. Animals. Cytokines / physiology. Epidermal Growth Factor / physiology. Heparin-binding EGF-like Growth Factor. Humans. Intercellular Signaling Peptides and Proteins. Intra-Abdominal Fat / physiology. Metabolic Syndrome X / physiopathology. Nicotinamide Phosphoribosyltransferase. Plasminogen Activator Inhibitor 1 / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 16311222.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Cytokines; 0 / HBEGF protein, human; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / Plasminogen Activator Inhibitor 1; 0 / Tumor Necrosis Factor-alpha; 62229-50-9 / Epidermal Growth Factor; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
  • [Number-of-references] 19
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50. Keophiphath M, Rouault C, Divoux A, Clément K, Lacasa D: CCL5 promotes macrophage recruitment and survival in human adipose tissue. Arterioscler Thromb Vasc Biol; 2010 Jan;30(1):39-45
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  • [Title] CCL5 promotes macrophage recruitment and survival in human adipose tissue.
  • OBJECTIVE: To examine the role of adipose-produced chemokine, chemokine ligand (CCL) 5, on the recruitment and survival of macrophages in human white adipose tissue (WAT).
  • CCL5, but not CCL2, secretion was higher in visceral compared to subcutaneous WAT.
  • CCL5 mRNA expression was positively correlated with the inflammatory macrophage markers as CD11b, tumor necrosis factor-alpha, and IL-6 in visceral WAT (n=24 obese subjects), and was higher in macrophages than other WAT cells.
  • Whereas in obese WAT apoptotic macrophages were located around necrotic adipocytes, we demonstrated that CCL5, but not CCL2, protected macrophages from free cholesterol-induced apoptosis via activation of the Akt/Erk pathways.
  • [MeSH-major] Adipose Tissue, White / immunology. Chemokine CCL5 / blood. Chemokine CCL5 / immunology. Inflammation / immunology. Macrophages / immunology. Obesity, Morbid / immunology
  • [MeSH-minor] Antigens, CD11b / metabolism. Apoptosis / immunology. Biopsy. Body Weight / immunology. Cell Adhesion / immunology. Cell Movement / immunology. Cell Survival / immunology. Female. Humans. Interleukin-6 / metabolism. RNA, Messenger / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19893003.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / CCL5 protein, human; 0 / Chemokine CCL5; 0 / IL6 protein, human; 0 / ITGAM protein, human; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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51. Skubitz KM, Cheng EY, Clohisy DR, Thompson RC, Skubitz AP: Differential gene expression in liposarcoma, lipoma, and adipose tissue. Cancer Invest; 2005;23(2):105-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in liposarcoma, lipoma, and adipose tissue.
  • Malignant transformation is thought to be associated with changes in the expression of a number of genes, and this alteration in gene expression is felt to be critical to the development of the malignant phenotype.
  • Sarcomas represent a diverse group of tumors derived from cells of mesenchymal origin.
  • In an effort to better understand the biology of liposarcomas, gene expression in normal adipose tissue, lipomas, and liposarcomas was examined using the Affymetrix microarray technology.
  • Differences in gene expression among normal adipose tissue, lipomas, and liposarcomas were observed.
  • In addition, genes expressed uniquely in liposarcoma among these and 18 other tissue sample sets were identified.
  • Gene sets were devised that allowed the separation of liposarcomas from other samples, and most normal adipose tissue from most lipomas using the Eisen clustering software "Cluster."
  • We conclude that differences in gene expression can be identified among different tumors derived from the adipocyte series.
  • Such differences in gene expression may help differentiate among subtypes of sarcomas, and may also yield clues to the pathophysiology of this heterogeneous group of tumors.
  • [MeSH-major] Adipose Tissue / physiology. Gene Expression Profiling. Lipoma / genetics. Liposarcoma / genetics. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Gene Expression Regulation, Developmental. Humans. Phenotype. Tumor Cells, Cultured

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  • (PMID = 15813502.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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52. Bodary PF: Links between adipose tissue and thrombosis in the mouse. Arterioscler Thromb Vasc Biol; 2007 Nov;27(11):2284-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Links between adipose tissue and thrombosis in the mouse.
  • A primary problem is that obese individuals are at increased risk of suffering from cardiovascular disease complications such as myocardial infarction and stroke.
  • Because fat accumulation is a consistent aspect of obesity, mechanisms that may link adipose tissue to cardiovascular disease complications should be considered.
  • Proteins expressed from adipose tissue, known as adipokines, are hypothesized to have important effects on the progression and incidence of cardiovascular disease complications.
  • This review examines the evidence that adipokines play a direct role in vascular thrombosis, an important event in cardiovascular disease complications.
  • [MeSH-major] Adipose Tissue / physiopathology. Obesity / blood. Thrombosis / blood
  • [MeSH-minor] Adiponectin / blood. Animals. Hemostasis. Leptin / blood. Mice. Plasminogen Activator Inhibitor 1 / blood. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17761944.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Adipoq protein, mouse; 0 / Leptin; 0 / Plasminogen Activator Inhibitor 1; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 99
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53. Gomillion CT, Burg KJ: Stem cells and adipose tissue engineering. Biomaterials; 2006 Dec;27(36):6052-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cells and adipose tissue engineering.
  • A large proportion of the plastic and reconstructive surgical procedures performed each year are to repair soft tissue defects that result from traumatic injury, tumor resection, and congenital defects.
  • These defects typically result from the loss of a large volume of adipose tissue.
  • Additionally, the success of using autologous fat tissue grafts to repair soft tissue defects has been limited.
  • Researchers are thus investigating strategies to engineer volumes of adipose tissue that may be used in these cases.
  • A necessary component for engineering a viable tissue construct is an appropriate cell source.
  • Attempts to engineer adipose tissue have involved the use of preadipocytes and adipocytes as the base cell source.
  • Increased interest surrounding the research and development of stem cells as a source of cells for tissue engineering has, however, led to a new path of investigation for developing adipose tissue-engineering strategies.
  • This manuscript serves as a review of the current state of adipose tissue-engineering methods and describes the shift toward tissue-engineering strategies using stem cells.
  • [MeSH-major] Adipocytes / cytology. Adipocytes / physiology. Adipose Tissue / cytology. Adipose Tissue / physiology. Stem Cells / cytology. Stem Cells / physiology. Tissue Engineering / methods
  • [MeSH-minor] Animals. Cell Culture Techniques / instrumentation. Cell Culture Techniques / methods. Cell Culture Techniques / trends. Cell Differentiation. Humans

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  • (PMID = 16973213.001).
  • [ISSN] 0142-9612
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] England
  • [Number-of-references] 128
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54. Chudek J, Wiecek A: Adipose tissue, inflammation and endothelial dysfunction. Pharmacol Rep; 2006;58 Suppl:81-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose tissue, inflammation and endothelial dysfunction.
  • During the last decade, white adipose tissue was recognized to be an active endocrine organ and a source of many proinflammatory cytokines, chemokines, growth factors and complement proteins.
  • As endothelial dysfunction is one of the early stages of atherosclerosis, it is reasonable to consider that substances secreted by adipose tissue may influence directly or indirectly (for instance by induction of microinflammation) the function of endothelial cells.
  • [MeSH-major] Adipose Tissue / metabolism. Endothelial Cells / metabolism
  • [MeSH-minor] Adiponectin / physiology. Atherosclerosis / etiology. Atherosclerosis / metabolism. Atherosclerosis / physiopathology. Cardiovascular Diseases / etiology. Cardiovascular Diseases / immunology. Cardiovascular Diseases / metabolism. Endothelium, Vascular / metabolism. Endothelium, Vascular / physiopathology. Humans. Inflammation / metabolism. Inflammation Mediators / metabolism. Interleukin-6 / metabolism. Leptin / physiology. Obesity / complications. Obesity / immunology. Obesity / metabolism. Plasminogen Activator Inhibitor 1 / metabolism. Renin-Angiotensin System / physiology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17332676.001).
  • [ISSN] 1734-1140
  • [Journal-full-title] Pharmacological reports : PR
  • [ISO-abbreviation] Pharmacol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Leptin; 0 / Plasminogen Activator Inhibitor 1; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 73
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55. Zahorska-Markiewicz B: Metabolic effects associated with adipose tissue distribution. Adv Med Sci; 2006;51:111-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolic effects associated with adipose tissue distribution.
  • Cardiovascular and metabolic risk depends not only on the overall obesity but also fat distribution is more powerfull predictor for risk factors.
  • Adipose tissue produces and secretes a variety of bioactive peptides - adipokines The most recently described adipocyte secretory proteins contribute to the pathogenesis of impaired insulin secretion and insulin resistance, endothelial dysfunction, a proinflammatory state and promote progression of atherosclerosis.
  • This review presents an overview of the adipose tissue secreted proteins (leptin, TNF-alpha, IL-6, adiponectin, resistin, visfatin, ASP, FIAF, MT) role and their regulation in the context of abdominal obesity and the adverse metabolic consequences.
  • [MeSH-major] Adipose Tissue / metabolism. Obesity / metabolism
  • [MeSH-minor] Adiponectin / metabolism. Animals. Humans. Interleukin-6 / metabolism. Leptin / metabolism. Resistin / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17357288.001).
  • [ISSN] 1896-1126
  • [Journal-full-title] Advances in medical sciences
  • [ISO-abbreviation] Adv Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Interleukin-6; 0 / Leptin; 0 / Resistin; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 35
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56. Franco-Pons N, Gea-Sorlí S, Closa D: Release of inflammatory mediators by adipose tissue during acute pancreatitis. J Pathol; 2010 Jun;221(2):175-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Release of inflammatory mediators by adipose tissue during acute pancreatitis.
  • Fat necrosis appears in the severe acute pancreatitis as a consequence of the release of lipolytic enzymes, but its potential role on the progression of the disease is unclear.
  • In this study, we have examined the role of white adipose tissue as a source of inflammatory mediators that can promote systemic inflammation during experimental taurocholate-induced acute pancreatitis in rats.
  • The inflammatory status and the expression of TNFalpha, iNOS, adiponectin and IL-10 were determined in necrotic and non-necrotic areas of adipose tissue.
  • Samples of adipose tissue were also used to induce the activation of macrophages in vitro.
  • A strong inflammatory infiltrate was observed in the border between necrotic and non-necrotic areas of adipose tissue.
  • Altogether, these results indicate that adipose tissue inflammation is a process secondary to acute pancreatitis but also contributes to the generation of mediators potentially involved in the induction of the systemic inflammatory response.
  • [MeSH-major] Adipose Tissue, White / metabolism. Fat Necrosis / metabolism. Inflammation Mediators / metabolism. Interleukin-10 / metabolism. Pancreatitis / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Acute Disease. Adiponectin / metabolism. Analysis of Variance. Animals. Disease Models, Animal. Macrophage Activation. Macrophages, Peritoneal / physiology. Male. Nitric Oxide Synthase Type II / metabolism. Rats. Rats, Wistar. Taurocholic Acid

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  • [Copyright] Copyright (c) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 20217859.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Inflammation Mediators; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 5E090O0G3Z / Taurocholic Acid; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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57. Sugita S, Kamei Y, Oka J, Suganami T, Ogawa Y: Macrophage-colony stimulating factor in obese adipose tissue: studies with heterozygous op/+ mice. Obesity (Silver Spring); 2007 Aug;15(8):1988-95
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  • [Title] Macrophage-colony stimulating factor in obese adipose tissue: studies with heterozygous op/+ mice.
  • We also examined the effect of decreased M-CSF signaling on the susceptibility to obesity and macrophage recruitment into the adipose tissue of mice.
  • RESEARCH METHODS AND PROCEDURES: The adipose tissue from mice with diet-induced obesity, obese KKA(y) mice, and ob/ob obese mice was used for RNA preparation.
  • Production of M-CSF and monocyte chemoattractant protein-1 (MCP-1) was examined by quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay.
  • The gene expression of macrophage markers in adipose tissue was examined.
  • RESULTS: The expression of M-CSF was not significantly changed in mice on a high-fat diet or in either type of genetic obesity (KKA(y) or ob/ob mice).
  • No change in the degree of obesity or macrophage-related gene expression (F4/80, CD68, and MCP-1) in the adipose tissue was observed in op/+ mice compared with +/+ control mice, which were either treated with a high-fat diet or crossed with KKA(y) mice.
  • DISCUSSION: This study demonstrated that there was no significant change in the expression of M-CSF in the adipose tissue from obese mice and only a minor phenotypic change, such as macrophage infiltration, in the adipose tissue from op/+ mice, suggesting that M-CSF does not play a major role in macrophage recruitment in the adipose tissue of obese mice.
  • [MeSH-minor] Animals. Antigens, Differentiation / biosynthesis. Antigens, Differentiation / genetics. Chemokine CCL2 / biosynthesis. Chemokine CCL2 / genetics. Crosses, Genetic. Histocytochemistry. Mice. Mice, Inbred C57BL. Mice, Obese. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptor, Macrophage Colony-Stimulating Factor / biosynthesis. Receptor, Macrophage Colony-Stimulating Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 17712116.001).
  • [ISSN] 1930-7381
  • [Journal-full-title] Obesity (Silver Spring, Md.)
  • [ISO-abbreviation] Obesity (Silver Spring)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Chemokine CCL2; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / monocyte-macrophage differentiation antigen; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
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58. Gu N, Han SP, Fei L, Pan XQ, Guo M, Chen RH, Guo XR: Resistin-binding peptide antagonizes role of resistin on white adipose tissue. Acta Pharmacol Sin; 2007 Feb;28(2):221-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resistin-binding peptide antagonizes role of resistin on white adipose tissue.
  • AIM: To investigate the direct effects of resistin and resistin-binding peptide (RBP) on lipid metabolism and endocrine function in adipose tissue.
  • METHODS: Rat white adipose tissue was cultured in vitro and incubated for 24 h with 30 ng/mL recombinant rat resistin protein (rResistin) or combined with RBP of varying concentrations(1x10(-12) mol/L, 1x10(-10) mol/L, 1x10(-8) mol/L).
  • Free fatty acids (FFA) released into medium was measured by a colorimetric kit.
  • The protein level and gene expression of TNF-alpha in adipose tissue were significantly increased after 24 h of exposure to rResistin, but only obviously decreased after incubated with 1x10(-8) mol/L RBP.
  • The levels of protein secretion and mRNA expression of adiponectin in adipose tissue were significantly decreased after 24 h of exposure to rResistin, but increased after incubated with RBP with the higher concentrations.
  • CONCLUSION: RBP can effectively antagonize the role of resistin on the lipid metabolism and endocrine function of adipose tissue.
  • [MeSH-major] Adipose Tissue, White / metabolism. Carrier Proteins / physiology. Resistin / physiology
  • [MeSH-minor] Adiponectin / genetics. Animals. Fatty Acids, Nonesterified / blood. Lipolysis. Male. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 17241525.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Carrier Proteins; 0 / Fatty Acids, Nonesterified; 0 / Resistin; 0 / Retn protein, rat; 0 / Tumor Necrosis Factor-alpha
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59. Paulmyer-Lacroix O, Desbriere R, Poggi M, Achard V, Alessi MC, Boudouresque F, Ouafik L, Vuaroqueaux V, Labuhn M, Dutourand A, Grino M: Expression of adrenomedullin in adipose tissue of lean and obese women. Eur J Endocrinol; 2006 Jul;155(1):177-85
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  • [Title] Expression of adrenomedullin in adipose tissue of lean and obese women.
  • OBJECTIVE: Adrenomedullin (AM), a potent vasodilatator and antioxidative peptide, was shown recently to be expressed by adipose tissue.
  • The aim of our study was to investigate the precise localization of AM within human adipose tissue, and to examine AM regulation in obesity.
  • DESIGN: Subcutaneous (SC) and omental (OM) adipose tissues from 9 lean and 13 obese women were profiled for AM expression changes.
  • Preadipocytes from human adipose tissue were isolated and differentiated under defined adipogenic conditions.
  • RESULTS: A strong AM expression was observed in vessel walls, stromal cell clusters and isolated stromal cells, some of them being CD 68 positive, whereas mature adipocytes were not labeled.
  • In vitro, preadipocytes of early differentiation stages spontaneously secreted AM.
  • No difference in AM localization was found between SC and OM adipose tissue.
  • AM levels in SC tissue did not differ between lean and obese subjects.
  • By contrast, AM levels in OM tissue were significantly higher in obese as compared with lean women.
  • Moreover, we found a positive relationship between OM AM and tumor necrosis factor alpha mRNA levels and AM-immunoreactive area in OM tissue followed the features of the metabolic syndrome.
  • CONCLUSION: Stromal cells from human adipose tissue, including macrophages, produce AM.

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  • (PMID = 16793965.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 148498-78-6 / Adrenomedullin
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60. Yu YH, Ginsberg HN: Adipocyte signaling and lipid homeostasis: sequelae of insulin-resistant adipose tissue. Circ Res; 2005 May 27;96(10):1042-52
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  • [Title] Adipocyte signaling and lipid homeostasis: sequelae of insulin-resistant adipose tissue.
  • For many years adipose tissue was viewed as the site where excess energy was stored, in the form of triglycerides (TGs), and where that energy, when needed elsewhere in the body, was released in the form of fatty acids (FAs).
  • Recently, it has become clear that when the regulation of the storage and release of energy by adipose tissue is impaired, plasma FA levels become elevated and excessive metabolism of FA, including storage of TGs, occurs in nonadipose tissues.
  • Most recently, work by several laboratories has made it clear that in addition to FA, adipose tissue communicates with the rest of the body by synthesizing and releasing a host of secreted molecules, collectively designated as adipokines.
  • In this review, we will describe, in detail, the effects of molecules secreted by adipose tissue, including FA, leptin, adiponectin, resistin, TNF-alpha, IL-6, and apolipoproteins, on lipid homeostasis in several nonadipose tissues, including liver, skeletal muscle, and pancreatic beta cells.
  • [MeSH-major] Adipocytes / metabolism. Adipose Tissue / metabolism. Insulin Resistance. Lipid Metabolism
  • [MeSH-minor] Adiponectin. Animals. Apolipoproteins / secretion. Fatty Acids / metabolism. Homeostasis. Hormones, Ectopic / physiology. Humans. Insulin / secretion. Intercellular Signaling Peptides and Proteins / physiology. Interleukin-6 / pharmacology. Islets of Langerhans / metabolism. Leptin / physiology. Lipoproteins, VLDL / metabolism. Liver / metabolism. Resistin. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 15920027.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK60530; United States / NHLBI NIH HHS / HL / R01 HL55638; United States / NHLBI NIH HHS / HL / R01 HL73030
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Apolipoproteins; 0 / Fatty Acids; 0 / Hormones, Ectopic; 0 / Insulin; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-6; 0 / Leptin; 0 / Lipoproteins, VLDL; 0 / RETN protein, human; 0 / Resistin; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 160
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61. Lambin S, van Bree R, Vergote I, Verhaeghe J: Chronic tumor necrosis factor-alpha infusion in gravid C57BL6/J mice accelerates adipose tissue development in female offspring. J Soc Gynecol Investig; 2006 Dec;13(8):558-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic tumor necrosis factor-alpha infusion in gravid C57BL6/J mice accelerates adipose tissue development in female offspring.
  • OBJECTIVE: Tumor necrosis factor (TNF)-alpha is thought to mediate, in part, the link between obesity and insulin resistance, and women with gestational diabetes mellitus (GDM) have raised serum TNF-alpha concentrations.
  • Our objective was to investigate whether systemic TNF-alpha administration into gravid C57BL6/J mice causes a GDM-like syndrome and affects growth and adipose tissue (AT) development in the offspring.
  • RESULTS: The peak glucose response to an intraperitoneal glucose stimulus in late-gravid mice and fetal weight were higher with 2 mug but not 4 mug rmTNF-alpha compared with saline; however, 2 mug TNF-alpha did not affect AT parameters.
  • The female but not male offspring of these mice showed accelerated growth, hyperadiposity, robustly increased leptin expression in all AT depots, and raised fasting blood glucose.
  • [MeSH-major] Adipose Tissue / drug effects. Cytokines / administration & dosage. Diabetes, Gestational / chemically induced. Fetal Development / drug effects. Tumor Necrosis Factor-alpha / administration & dosage

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  • (PMID = 17088083.001).
  • [ISSN] 1556-7117
  • [Journal-full-title] Journal of the Society for Gynecologic Investigation
  • [ISO-abbreviation] J. Soc. Gynecol. Investig.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha
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62. Kim KY, Kim HY, Kim JH, Lee CH, Kim DH, Lee YH, Han SH, Lim JS, Cho DH, Lee MS, Yoon S, Kim KI, Yoon DY, Yang Y: Tumor necrosis factor-alpha and interleukin-1beta increases CTRP1 expression in adipose tissue. FEBS Lett; 2006 Jul 10;580(16):3953-60
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  • [Title] Tumor necrosis factor-alpha and interleukin-1beta increases CTRP1 expression in adipose tissue.
  • CTRP1 is expressed at high levels in adipose tissues of LPS-stimulated Sprague-Dawley rats.
  • Also, a high level of expression of CTRP1 mRNA was observed in adipose tissues of Zucker diabetic fatty (fa/fa) rats, compared to Sprague-Dawley rats in the absence of LPS stimulation.
  • These findings indicate that CTRP1 expression may be associated with a low-grade chronic inflammation status in adipose tissues.
  • [MeSH-major] Adipokines / metabolism. Adipose Tissue / drug effects. Gene Expression Regulation / drug effects. Interleukin-1 / pharmacology. Proteins / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Differentiation. Cloning, Molecular. DNA, Complementary / genetics. Gene Expression Profiling. Humans. Lipopolysaccharides / pharmacology. Male. Mice. Molecular Sequence Data. Obesity. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Rats, Zucker. Sequence Alignment

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  • (PMID = 16806199.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adipokines; 0 / C1QTNF1 protein, human; 0 / CTRP1 protein, mouse; 0 / CTRP1 protein, rat; 0 / DNA, Complementary; 0 / Interleukin-1; 0 / Lipopolysaccharides; 0 / Proteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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63. Patrick CW, Uthamanthil R, Beahm E, Frye C: Animal models for adipose tissue engineering. Tissue Eng Part B Rev; 2008 Jun;14(2):167-78
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  • [Title] Animal models for adipose tissue engineering.
  • There is a critical need for adequate reconstruction of soft tissue defects resulting from tumor resection, trauma, and congenital abnormalities.
  • To be sure, adipose tissue engineering strategies offer promising solutions.
  • The aim of this review is to provide an overview of animal models currently employed for adipose tissue engineering.

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  • (PMID = 18544014.001).
  • [ISSN] 1937-3376
  • [Journal-full-title] Tissue engineering. Part B, Reviews
  • [ISO-abbreviation] Tissue Eng Part B Rev
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 71
  • [Other-IDs] NLM/ PMC2962856
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64. Okada T, Nishizawa H, Kurata A, Tamba S, Sonoda M, Yasui A, Kuroda Y, Hibuse T, Maeda N, Kihara S, Hadama T, Tobita K, Akamatsu S, Maeda K, Shimomura I, Funahashi T: URB is abundantly expressed in adipose tissue and dysregulated in obesity. Biochem Biophys Res Commun; 2008 Mar 7;367(2):370-6
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  • [Title] URB is abundantly expressed in adipose tissue and dysregulated in obesity.
  • URB/DRO1 contains N-terminal signal sequence and is thought to play a role in apoptosis of tumor cells.
  • In the present study, we investigated the expression pattern of URB mRNA in adipose tissue and secretion from cultured adipocytes.
  • In human and mouse, URB mRNA was predominantly expressed in adipose tissue and was downregulated in obese mouse models, such as ob/ob, KKAy, and diet-induced obese mice.
  • [MeSH-major] Adipose Tissue / metabolism. Glycoproteins / metabolism. Obesity / metabolism
  • [MeSH-minor] 3T3-L1 Cells. Animals. Down-Regulation. Female. Gene Expression Profiling. Gene Expression Regulation. Humans. Intercellular Signaling Peptides and Proteins. Mice. Mice, Inbred C57BL. Organ Specificity. Species Specificity. Tissue Distribution. Tumor Suppressor Proteins


65. Dray C, Daviaud D, Guigné C, Valet P, Castan-Laurell I: Caffeine reduces TNFalpha up-regulation in human adipose tissue primary culture. J Physiol Biochem; 2007 Dec;63(4):329-36
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  • [Title] Caffeine reduces TNFalpha up-regulation in human adipose tissue primary culture.
  • Adipose tissue secretions play an important role in the development of obesity-related pathologies such as diabetes.
  • Through inflammatory cytokines production, adipose tissue stromavascular fraction cells (SVF), and essentially macrophages, promote adipocyte insulin resistance by a paracrine way.
  • Since xanthine family compounds such as caffeine were shown to decrease inflammatory production by human blood cells, we investigated the possible effect of caffeine on Tumor Necrosis Factor alpha (TNFalpha) and Interleukin-6 (IL-6) expression by human adipose tissue primary culture.
  • For that purpose, human subcutaneous adipose tissue obtained from healthy non-obese women (BMI: 26.7 +/- 2.2 kg/m2) after abdominal dermolipectomy, was split into explants and cultured for 6 hours with or without caffeine.
  • Thus, caffeine, by decreasing TNFalpha expression, could improve adipose tissue inflammation during obesity.
  • [MeSH-major] Caffeine / pharmacology. Subcutaneous Fat / metabolism. Tumor Necrosis Factor-alpha / genetics. Up-Regulation

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  • (PMID = 18457008.001).
  • [ISSN] 1138-7548
  • [Journal-full-title] Journal of physiology and biochemistry
  • [ISO-abbreviation] J. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 3G6A5W338E / Caffeine
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66. Kos K, Harte AL, James S, Snead DR, O'Hare JP, McTernan PG, Kumar S: Secretion of neuropeptide Y in human adipose tissue and its role in maintenance of adipose tissue mass. Am J Physiol Endocrinol Metab; 2007 Nov;293(5):E1335-40
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  • [Title] Secretion of neuropeptide Y in human adipose tissue and its role in maintenance of adipose tissue mass.
  • NPY is an important central orexigenic hormone, but little is known about its peripheral actions in human adipose tissue (AT) or its potential paracrine effects.
  • Adipose-derived NPY mediates reduction of leptin secretion and may have implications for central feedback of adiposity signals.
  • [MeSH-minor] Adipocytes / physiology. Adult. Blotting, Western. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunohistochemistry. Leptin / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 17785501.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 0 / Leptin; 0 / Neuropeptide Y; 0 / PPAR gamma; 0 / Thiazolidinediones; 0 / Tumor Necrosis Factor-alpha; 05V02F2KDG / rosiglitazone
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67. Lira FS, Rosa JC, Zanchi NE, Yamashita AS, Lopes RD, Lopes AC, Batista ML Jr, Seelaender M: Regulation of inflammation in the adipose tissue in cancer cachexia: effect of exercise. Cell Biochem Funct; 2009 Mar;27(2):71-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of inflammation in the adipose tissue in cancer cachexia: effect of exercise.
  • The paraneoplastic syndrome of cachexia is considered a degenerative chronic inflammatory disease, being deeply related to the increase of pro-inflammatory factors, especially tumour necrosis factor alpha (TNF-alpha).
  • It is known that the adipose tissue is affected by cachexia and contributing with the secretion of pro-inflammatory factors which reach the adjacent tissues and the circulation.
  • The IL-10/TNF-alpha ratio has been recently postulated as a marker for the assessment of the degree of inflammation, which correlates with disease-associated morbidity and mortality.
  • In order to counteract inflammation in chronic disease, our group has currently adopted chronic endurance exercise in models of cancer cachexia and chronic heart failure.
  • Since it is clear that white adipose tissue is strongly implicated in the secretion of both pro- and anti-inflammatory factors in disease, we chose to address its contribution to cachexia-related inflammation and the effect of endurance training on the capacity of cytokine expression and secretion by this tissue.
  • Our results show an enhancement of IL-10 adipose tissue content, and increased IL-10/TNF-alpha ratio induced by endurance training.
  • [MeSH-major] Adipose Tissue / metabolism. Cachexia / metabolism. Exercise / physiology. Inflammation / metabolism. Neoplasms / physiopathology
  • [MeSH-minor] Animals. Cytokines / metabolism. Exercise Therapy. Humans. Interleukin-10 / metabolism. Signal Transduction / physiology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19226603.001).
  • [ISSN] 1099-0844
  • [Journal-full-title] Cell biochemistry and function
  • [ISO-abbreviation] Cell Biochem. Funct.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
  • [Number-of-references] 55
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68. Johnson MW, Lin D, Smir BN, Burger PC: Lipoglioblastoma: a lipidized glioma radiologically and histologically mimicking adipose tissue. World Neurosurg; 2010 Feb;73(2):108-11
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  • [Title] Lipoglioblastoma: a lipidized glioma radiologically and histologically mimicking adipose tissue.
  • BACKGROUND: We report the case of a man with glioblastoma containing a component radiologically and histologically mimicking adipose tissue.
  • CASE DESCRIPTION: A 48-year-old man recently complaining of headaches and difficulty with speech presented with a cystic peripherally enhancing left temporoparietal mass with focal intrinsically (precontrast) bright nodules in fluid attenuated inversion recovery and T1-weighted images similar to adipose tissue.
  • Histologically, the enhancing component was classic glioblastoma, whereas the bright nodules comprised tumor cells that in aggregate closely resembled adipose tissue.
  • CONCLUSIONS: The case illustrates the extent to which lipidized central nervous system tumors of glial origin, or components thereof, can radiologically and histologically resemble adipose tissue.
  • [MeSH-major] Adipose Tissue / pathology. Brain Neoplasms / pathology. Brain Neoplasms / radiography. Glioblastoma / pathology. Glioblastoma / radiography. Lipidoses / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20860936.001).
  • [ISSN] 1878-8769
  • [Journal-full-title] World neurosurgery
  • [ISO-abbreviation] World Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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69. Galic S, Oakhill JS, Steinberg GR: Adipose tissue as an endocrine organ. Mol Cell Endocrinol; 2010 Mar 25;316(2):129-39
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose tissue as an endocrine organ.
  • Obesity is characterized by increased storage of fatty acids in an expanded adipose tissue mass and is closely associated with the development of insulin resistance in peripheral tissues such as skeletal muscle and the liver.
  • In addition to being the largest source of fuel in the body, adipose tissue and resident macrophages are also the source of a number of secreted proteins.
  • Cloning of the obese gene and the identification of its product, leptin, was one of the first discoveries of an adipocyte-derived signaling molecule and established an important role for adipose tissue as an endocrine organ.
  • Adiponectin acts to increase insulin sensitivity, fatty acid oxidation, as well as energy expenditure and reduces the production of glucose by the liver.
  • More recently it has been acknowledged that macrophages are an important part of the secretory function of adipose tissue and the main source of inflammatory cyokines, such as TNFalpha and IL-6.
  • These proteins commonly known as adipokines are central to the dynamic control of energy metabolism, communicating the nutrient status of the organism with the tissues responsible for controlling both energy intake and expenditure as well as insulin sensitivity.
  • [MeSH-major] Adipose Tissue / physiology. Endocrine Glands / physiology
  • [MeSH-minor] Adiponectin / chemistry. Adiponectin / genetics. Adiponectin / metabolism. Animals. Energy Metabolism / physiology. Humans. Insulin Resistance / physiology. Interleukin-6 / metabolism. Leptin / genetics. Leptin / metabolism. Macrophages / cytology. Macrophages / metabolism. Obesity / metabolism. Obesity / physiopathology. Protein Conformation. Resistin / chemistry. Resistin / genetics. Resistin / metabolism. Retinol-Binding Proteins, Plasma / genetics. Retinol-Binding Proteins, Plasma / metabolism. Signal Transduction / physiology. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19723556.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Interleukin-6; 0 / Leptin; 0 / RBP4 protein, human; 0 / Resistin; 0 / Retinol-Binding Proteins, Plasma; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 157
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70. Lin G, Yang R, Banie L, Wang G, Ning H, Li LC, Lue TF, Lin CS: Effects of transplantation of adipose tissue-derived stem cells on prostate tumor. Prostate; 2010 Jul 1;70(10):1066-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of transplantation of adipose tissue-derived stem cells on prostate tumor.
  • The present study tested the hypothesis that stromal cells of the adipose tissue might be recruited by cancer cells to help tumor growth.
  • One week later, adipose tissue-derived stromal or stem cells (ADSC) or phosphate-buffered saline (PBS, as control) was transplanted similarly to the left flank.
  • Tumor size was monitored for the next 34 days; afterwards, the mice were sacrificed and their tumors harvested for histological examination.
  • The involvement of the CXCL12/CXCR4 axis was tested by migration assay in the presence of a specific inhibitor AMD3100.
  • RESULTS: Throughout the entire course, the average size of PC3 tumors in ADSC-treated mice was larger than in PBS-treated mice.
  • ADSC were identified inside the tumors of ADSC-treated mice; CXCR4 expression was also detected.
  • Capillary density was twice as high in the tumors of ADSC-treated mice than in the tumors of PBS-treated mice.
  • VEGF expression was similar but FGF2 expression was significantly higher in tumors of ADSC-treated mice than in the tumors of PBS-tread mice.
  • ADSC helps tumor growth by increasing tumor vascularity, and which was mediated by FGF2.

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  • (PMID = 20232361.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK045370; United States / NIDDK NIH HHS / DK / DK045370-13; United States / NIDDK NIH HHS / DK / R37 DK045370-13; United States / NIDDK NIH HHS / DK / R37 DK045370; United States / NIDDK NIH HHS / DK / R01 DK045370
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCR4 protein, mouse; 0 / Chemokine CXCL12; 0 / Cxcl12 protein, mouse; 0 / Heterocyclic Compounds; 0 / Receptors, CXCR4; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 103107-01-3 / Fibroblast Growth Factor 2; 155148-31-5 / JM 3100
  • [Other-IDs] NLM/ NIHMS196734; NLM/ PMC2877148
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71. Axelsson J, Heimbürger O, Lindholm B, Stenvinkel P: Adipose tissue and its relation to inflammation: the role of adipokines. J Ren Nutr; 2005 Jan;15(1):131-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose tissue and its relation to inflammation: the role of adipokines.
  • An activated inflammatory response is a common feature of end-stage renal disease (ESRD) patients and predicts outcome.
  • Adipose tissue is a complex organ with functions far beyond the mere storage of energy and secretes a number of proinflammatory adipokines, such as leptin, resistin, tumor necrosis factor-alpha and interleukin-6, as well as one anti-inflammatory adipokine, adiponectin.
  • It has been proposed that adipose tissue may be a significant contributor to increased systemic inflammation in nonrenal patients.
  • [MeSH-major] Adiponectin / physiology. Adipose Tissue / physiopathology. Cytokines / physiology. Inflammation / physiopathology. Kidney Failure, Chronic / complications. Leptin / physiology
  • [MeSH-minor] Body Composition. Body Mass Index. Cardiovascular Diseases / epidemiology. Humans. Infection / complications. Interleukin-6 / physiology. Obesity / complications. Renal Dialysis. Resistin / physiology. Risk Factors. Tumor Necrosis Factor-alpha / physiology. Wasting Syndrome

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  • (PMID = 15648022.001).
  • [ISSN] 1532-8503
  • [Journal-full-title] Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation
  • [ISO-abbreviation] J Ren Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Cytokines; 0 / Interleukin-6; 0 / Leptin; 0 / Resistin; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 47
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72. López Fontana C, Maselli Artola ME, Vanrell Rodríguez MC, Di Milta Mónaco NA, Pérez Elizalde R, López Laur JD: [Advances on the influence of adipose tissue on prostate cancer]. Actas Urol Esp; 2009 Mar;33(3):242-8
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  • [Title] [Advances on the influence of adipose tissue on prostate cancer].
  • [Transliterated title] Avances sobre la influencia del tejido adiposo en el adenocarcinoma de próstata.
  • Numerous studies have investigated the association between obesity and prostate cancer (CaP), although the results have not been concluding due to the great difficulty to evaluate the effects of obesity on the development of this type of tumor.
  • The aim of this study was to carry out a comprehensive over-view of the existing evidence about the role of adipose tissue in the prostate carcinogenesis.
  • CONCLUSION: Obesity may promote the progression of established PC rather than being a risk factor for the development of this tumour.
  • However, additional studies are needed to clarify the relationship between adipokines and PC before developing new preventive or treatment strategies for this tumor.
  • [MeSH-major] Adipose Tissue / physiology. Obesity / complications. Prostatic Neoplasms / etiology


73. Kolokol'chikova EG, Pal'tsyn AA, Shchegolev AI, Adamyan AA, Chervonskaya NV: Proliferative activity of adipocytes in adipose tissue tumors. Bull Exp Biol Med; 2005 Jul;140(1):122-6
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  • [Title] Proliferative activity of adipocytes in adipose tissue tumors.
  • Electron-autoradiographic study of normal and tumor-transformed adipose tissue (common lipoma and destructive lipoma, i.e. infiltrating and degrading lipoma) showed the capacity of adipose tissue cells in lipomas, especially in destructive lipomas, to proliferation and differentiation.
  • In vivo synthesis of DNA in mature adipocytes not observed previously is described.
  • The role of microvascular wall cells as mesenchymal multipotent precursors in the formation of the adipose tissue is discussed.
  • [MeSH-major] Adipocytes / ultrastructure. Cell Differentiation. Cell Proliferation. Lipoma / physiopathology

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  • (PMID = 16254637.001).
  • [ISSN] 0007-4888
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 10028-17-8 / Tritium
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74. Tsuzuki T, Kawakami Y, Suzuki Y, Abe R, Nakagawa K, Miyazawa T: Intake of conjugated eicosapentaenoic acid suppresses lipid accumulation in liver and epididymal adipose tissue in rats. Lipids; 2005 Nov;40(11):1117-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intake of conjugated eicosapentaenoic acid suppresses lipid accumulation in liver and epididymal adipose tissue in rats.
  • Compared with other groups, rats fed CEPA showed a significant weight loss in epididymal adipose tissue and significant decreases in the levels of liver TAG and total cholesterol (TC), indicating reduced accumulation of lipid in the liver and adipose tissue.
  • The plasma levels of TAG, TC, FFA, and tumor necrosis factor-alpha in rats fed CEPA were reduced, as was the activity of the FA synthesis system in the liver, whereas the FA-beta-oxidation system was activated by CEPA.
  • These results suggest that intake of CEPA suppresses lipid accumulation in the liver and epididymal adipose tissue while increasing lipid catabolism in rats.
  • [MeSH-major] Adipose Tissue / metabolism. Eicosapentaenoic Acid / physiology. Lipid Metabolism. Liver / metabolism
  • [MeSH-minor] Animals. Fatty Acids, Nonesterified / blood. Leptin / blood. Linoleic Acids, Conjugated / physiology. Male. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16459923.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Nonesterified; 0 / Leptin; 0 / Linoleic Acids, Conjugated; 0 / Tumor Necrosis Factor-alpha; AAN7QOV9EA / Eicosapentaenoic Acid
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75. Jager J, Grémeaux T, Gonzalez T, Bonnafous S, Debard C, Laville M, Vidal H, Tran A, Gual P, Le Marchand-Brustel Y, Cormont M, Tanti JF: Tpl2 kinase is upregulated in adipose tissue in obesity and may mediate interleukin-1beta and tumor necrosis factor-{alpha} effects on extracellular signal-regulated kinase activation and lipolysis. Diabetes; 2010 Jan;59(1):61-70
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  • [Title] Tpl2 kinase is upregulated in adipose tissue in obesity and may mediate interleukin-1beta and tumor necrosis factor-{alpha} effects on extracellular signal-regulated kinase activation and lipolysis.
  • OBJECTIVE: Activation of extracellular signal-regulated kinase-(ERK)-1/2 by cytokines in adipocytes is involved in the alterations of adipose tissue functions participating in insulin resistance.
  • This study aims at identifying proteins regulating ERK1/2 activity, specifically in response to inflammatory cytokines, to provide new insights into mechanisms leading to abnormal adipose tissue function.
  • Gene expression in adipocytes and adipose tissue of obese mice and subjects was measured by real-time PCR.
  • RESULTS: IkappaB kinase-(IKK)-beta inhibition prevented mitogen-activated protein (MAP) kinase kinase (MEK)/ERK1/2 activation in response to interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha but not insulin in 3T3-L1 and human adipocytes, suggesting that IKKbeta regulated a MAP kinase kinase kinase (MAP3K) involved in ERK1/2 activation induced by inflammatory cytokines.
  • Pharmacological inhibition or silencing of Tpl2 prevented MEK/ERK1/2 activation by these cytokines but not by insulin, demonstrating its involvement in ERK1/2 activation specifically in response to inflammatory stimuli.
  • Tpl2 mRNA expression was upregulated in adipose tissue of obese mice and patients and correlated with TNF-alpha expression.
  • The deregulated expression of Tpl2 in adipose tissue suggests that Tpl2 may be a new actor in adipose tissue dysfunction in obesity.
  • [MeSH-major] 3T3-L1 Cells / cytology. Adipocytes / cytology. Interleukin-1beta / pharmacology. MAP Kinase Kinase Kinases / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins / genetics. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Differentiation. Enzyme Activation. Fasting. Humans. I-kappa B Kinase / metabolism. Lipolysis. Male. Mice. Mice, Inbred C57BL. Mice, Inbred NOD. Mice, Obese. Obesity, Morbid / physiopathology. Reverse Transcriptase Polymerase Chain Reaction. Thinness. Up-Regulation

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  • (PMID = 19808894.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Proto-Oncogene Proteins; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / Ikbkb protein, mouse; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / Map3k8 protein, mouse
  • [Other-IDs] NLM/ PMC2797946
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76. Lindegaard B, Larsen LF, Hansen AB, Gerstoft J, Pedersen BK, Reue K: Adipose tissue lipin expression levels distinguish HIV patients with and without lipodystrophy. Int J Obes (Lond); 2007 Mar;31(3):449-56
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  • [Title] Adipose tissue lipin expression levels distinguish HIV patients with and without lipodystrophy.
  • Its pathophysiology is not well understood, but has been linked to antiadipogenic effects of antiretroviral drugs.
  • Lipin represents a newly characterized protein that is critical for adipocyte differentiation, and lipin deficiency leads to lipodystrophy in the mouse.
  • DESIGN: We measured lipin mRNA levels in subcutaneous abdominal and femoral-gluteal adipose tissue biopsies from HIV-infected patients with or without lipodystrophy, and in healthy controls.
  • In addition, lipin expression levels were inversely correlated with adipose tissue expression of inflammatory cytokines interleukin (IL)-6, IL-8 and IL-18, which typically increase in HIV-associated lipoatrophy.
  • Based on the demonstrated role for lipin in promoting lipogenic gene expression, these observations raise the possibility that variations in lipin levels may contribute to variations in adipose tissue mass and function that distinguish HIV patients with and without lipodystrophy.
  • [MeSH-major] Adipose Tissue / metabolism. HIV Infections / metabolism. Nuclear Proteins / analysis
  • [MeSH-minor] Cross-Sectional Studies. Extremities. Gene Expression / genetics. HIV-Associated Lipodystrophy Syndrome / genetics. HIV-Associated Lipodystrophy Syndrome / metabolism. Humans. Interleukins / analysis. Isomerism. Male. Middle Aged. Phosphatidate Phosphatase. RNA, Messenger / analysis. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16847472.001).
  • [ISSN] 0307-0565
  • [Journal-full-title] International journal of obesity (2005)
  • [ISO-abbreviation] Int J Obes (Lond)
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL28481
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.1.3.4 / LPIN1 protein, human; EC 3.1.3.4 / Phosphatidate Phosphatase
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77. Madec S, Chiarugi M, Santini E, Rossi C, Miccoli P, Ferrannini E, Solini A: Pattern of expression of inflammatory markers in adipose tissue of untreated hypertensive patients. J Hypertens; 2010 Jul;28(7):1459-65
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  • [Title] Pattern of expression of inflammatory markers in adipose tissue of untreated hypertensive patients.
  • OBJECTIVE: Adiposity contributes to the insulin resistance and endothelial dysfunction of the hypertensive state; the inflammatory network and the metalloprotease (MMP)/ tissue inhibitor of metalloprotease (TIMP) system modulate vascular structure and function.
  • METHODS: We measured interleukin-6 (IL-6); plasminogen activator inhibitor-1 (PAI-1); tumor necrosis factor-alpha; transforming growth factor-beta; MMP-2, MMP-9, TIMP-1, and TIMP-2 expression; MMP-2 and MMP-9 activity; and TIMP-1 and TIMP-2 protein in adipocytes isolated from paired samples of visceral and subcutaneous adipose tissue of 30 nonobese, untreated hypertensive patients and 20 normotensive controls.
  • RESULTS: Although expression of IL-6, PAI-1, tumor necrosis factor-alpha, and transforming growth factor-beta were generally higher in visceral adipocytes, IL-6, PAI-1, and tumor necrosis factor-alpha were overexpressed, and transforming growth factor-beta was underexpressed in hypertensive vs. controls (all P<0.0001).
  • MMP-2 and TIMP-2 expression - which were higher in subcutaneous than visceral cells - were reduced in hypertensive patients (all P<0.0001), whereas MMP-9 and TIMP-1 did not differ between the two groups.
  • [MeSH-major] Adipose Tissue / metabolism. Hypertension / metabolism. Inflammation / metabolism. Inflammation Mediators / metabolism
  • [MeSH-minor] Aged. Biomarkers / analysis. Case-Control Studies. Female. Humans. Interleukin-6 / analysis. Male. Matrix Metalloproteinase 9 / analysis. Matrix Metalloproteinases / analysis. Matrix Metalloproteinases / metabolism. Middle Aged. Obesity / metabolism. Plasminogen Activator Inhibitor 1 / analysis. Plasminogen Activator Inhibitor 1 / blood. Subcutaneous Tissue / metabolism. Tissue Inhibitor of Metalloproteinase-1 / analysis. Tissue Inhibitor of Metalloproteinase-1 / blood. Tissue Inhibitor of Metalloproteinase-2 / analysis. Transforming Growth Factor beta / analysis. Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / pharmacology. Tumor Necrosis Factor-alpha / analysis. Tumor Necrosis Factor-alpha / metabolism

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  • [CommentIn] J Hypertens. 2010 Jul;28(7):1377-9 [20574246.001]
  • (PMID = 20589975.001).
  • [ISSN] 1473-5598
  • [Journal-full-title] Journal of hypertension
  • [ISO-abbreviation] J. Hypertens.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Plasminogen Activator Inhibitor 1; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.35 / Matrix Metalloproteinase 9
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78. Pontikides N, Krassas GE: Basic endocrine products of adipose tissue in states of thyroid dysfunction. Thyroid; 2007 May;17(5):421-31
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  • [Title] Basic endocrine products of adipose tissue in states of thyroid dysfunction.
  • Over the past decade it has been established that adipose tissue is capable of secreting a variety of hormones, cytokines, growth factors, and other peptides that are capable of changing adipocyte biology as well as different organ systems, like the central nervous system, liver, pancreas, and skeletal muscles.
  • The aim of this review is to summarize our current knowledge on the role of basic peptides of adipose tissue, such as adiponectin, interleukin-6, tumor necrosis factor-alpha, and resistin, in states of altered thyroid function.
  • [MeSH-major] Adiponectin / physiology. Adipose Tissue / metabolism. Hyperthyroidism / metabolism. Hypothyroidism / metabolism. Interleukin-6 / physiology. Resistin / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 17542672.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Interleukin-6; 0 / Resistin; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 82
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79. Xue Y, Cao R, Nilsson D, Chen S, Westergren R, Hedlund EM, Martijn C, Rondahl L, Krauli P, Walum E, Enerbäck S, Cao Y: FOXC2 controls Ang-2 expression and modulates angiogenesis, vascular patterning, remodeling, and functions in adipose tissue. Proc Natl Acad Sci U S A; 2008 Jul 22;105(29):10167-72
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  • [Title] FOXC2 controls Ang-2 expression and modulates angiogenesis, vascular patterning, remodeling, and functions in adipose tissue.
  • Here we show that in a transgenic mouse model, increased expression of forkhead box C2 (FOXC2) in the adipose tissue affects angiogenesis, vascular patterning, and functions.
  • White and brown adipose tissues contain a considerably high density of microvessels appearing as vascular plexuses, which show redistribution of vascular smooth muscle cells and pericytes.
  • Thus, the FOXC2-Ang-2 signaling system is crucial for controlling adipose vascular function, which is part of an adaptation to increased adipose tissue metabolism.
  • [MeSH-major] Adipose Tissue / blood supply. Adipose Tissue / physiology. Angiopoietin-2 / genetics. Forkhead Transcription Factors / physiology
  • [MeSH-minor] Adipocytes / metabolism. Adipogenesis / genetics. Adipogenesis / physiology. Adipose Tissue, Brown / blood supply. Adipose Tissue, Brown / physiology. Animals. Gene Expression Regulation. Mice. Mice, Transgenic. Neovascularization, Physiologic / genetics. Phenotype. Promoter Regions, Genetic. Signal Transduction

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  • (PMID = 18621714.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiopoietin-2; 0 / Forkhead Transcription Factors; 0 / mesenchyme fork head 1 protein
  • [Other-IDs] NLM/ PMC2481379
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80. Cavarretta IT, Altanerova V, Matuskova M, Kucerova L, Culig Z, Altaner C: Adipose tissue-derived mesenchymal stem cells expressing prodrug-converting enzyme inhibit human prostate tumor growth. Mol Ther; 2010 Jan;18(1):223-31
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  • [Title] Adipose tissue-derived mesenchymal stem cells expressing prodrug-converting enzyme inhibit human prostate tumor growth.
  • The ability of human adipose tissue-derived mesenchymal stem cells (AT-MSCs), engineered to express the suicide gene cytosine deaminase::uracil phosphoribosyltransferase (CD::UPRT), to convert the relatively nontoxic 5-fluorocytosine (5-FC) into the highly toxic antitumor 5-fluorouracil (5-FU) together with their ability to track and engraft into tumors and micrometastases makes these cells an attractive tool to activate prodrugs directly within the tumor mass.
  • In a pilot preclinical study, we observed that coinjections of human bone metastatic PC cells along with the transduced AT-MSCs into nude mice treated with 5-FC induced a complete tumor regression in a dose dependent manner or did not even allow the establishment of the tumor.
  • More importantly, we also demonstrated that the therapeutic cells were effective in significantly inhibiting PC tumor growth after intravenous administration that is a key requisite for any clinical application of gene-directed enzyme prodrug therapies.
  • [MeSH-major] Cytosine Deaminase / physiology. Mesenchymal Stromal Cells / metabolism. Mesenchymal Stromal Cells / physiology. Pentosyltransferases / physiology. Prostatic Neoplasms / therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Flucytosine / pharmacology. Fluorouracil / pharmacology. Humans. Male. Mice. Mice, Nude

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  • (PMID = 19844197.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] D83282DT06 / Flucytosine; EC 2.4.2.- / Pentosyltransferases; EC 2.4.2.9 / uracil phosphoribosyltransferase; EC 3.5.4.1 / Cytosine Deaminase; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2839205
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81. Axelsson J, Heimbürger O, Stenvinkel P: Adipose tissue and inflammation in chronic kidney disease. Contrib Nephrol; 2006;151:165-74
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  • [Title] Adipose tissue and inflammation in chronic kidney disease.
  • Cardiovascular disease remains a major cause of morbidity and mortality in end-stage renal disease patients.
  • As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of cardiovascular disease in this high-risk population, inflammation (interrelated to insulin resistance, oxidative stress, wasting and endothelial dysfunction) has been suggested to be a significant contributor.
  • Recent studies show that the adipose tissue is a complex organ with functions far beyond the mere storage of energy.
  • Indeed, it has been shown that fat tissue secretes a number of adipokines including leptin, adiponectin and visfatin, as well as a cytokines (here defined as signaling proteins mainly secreted by other cells present in adipose tissue, but sometimes also to a lesser degree by adipocytes per se), such as resistin, tumor-necrosis factor-alpha and interleukin-6.
  • Adipokine serum levels are markedly elevated in chronic kidney disease, probably due to decreased renal excretion.
  • Much research is thus still needed to elucidate the likely complex interactions between different fat tissue depots, muscle tissue and its' effects on inflammation, vascular health and outcome in this high-risk population.
  • [MeSH-major] Adipose Tissue / immunology. Cardiovascular Diseases / immunology. Inflammation / immunology. Kidney Failure, Chronic / immunology

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  • (PMID = 16929140.001).
  • [ISSN] 0302-5144
  • [Journal-full-title] Contributions to nephrology
  • [ISO-abbreviation] Contrib Nephrol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 59
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82. Qian YW, Gao JH, Lu F, Zheng XD: [The differences between adipose tissue derived stem cells and lipoma mesenchymal stem cells in characteristics]. Zhonghua Zheng Xing Wai Ke Za Zhi; 2010 Mar;26(2):125-32
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  • [Title] [The differences between adipose tissue derived stem cells and lipoma mesenchymal stem cells in characteristics].
  • OBJECTIVE: To compared the biological characteristics of adipose-derived stem cells and lipoma-derived mesenchymal stem cells (LMSCs) in vitro, so as to assess the safety of adipose-derived stem cells( ASCs) for transplantation.
  • METHODS: Regular slice and stain of adipose and lipoma tissue were performed.
  • ASCs and LMSCs were isolation from the two tissues by enzymatic digestion, and the appearance of the cultured cells was observed.
  • QRT-PCR was used to detect the expression of tumor-specific gene (the high-mobility group AT-hook 2, HMGA2), and immunocytochemistry was used to detect the expression of telomerase.
  • RESULTS: Marked difference was observed in histologic sections of adipose tissue and lipoma tissue.
  • ASCs showed a good consistent in cell morphology while LMSCs not.
  • [MeSH-major] Adipose Tissue / cytology. Lipoma / pathology. Stem Cells / cytology

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  • (PMID = 20540318.001).
  • [ISSN] 1009-4598
  • [Journal-full-title] Zhonghua zheng xing wai ke za zhi = Zhonghua zhengxing waike zazhi = Chinese journal of plastic surgery
  • [ISO-abbreviation] Zhonghua Zheng Xing Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] China
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83. Ramsay TG, Caperna TJ: Ontogeny of adipokine expression in neonatal pig adipose tissue. Comp Biochem Physiol B Biochem Mol Biol; 2009 Jan;152(1):72-8
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  • [Title] Ontogeny of adipokine expression in neonatal pig adipose tissue.
  • This study examined ontogeny of development for a range of adipokines in neonatal adipose tissue.
  • Pigs (Sus scrofa) were selected across six litters for sampling subcutaneous (SQ) and perirenal (PR) adipose tissues at d1, d4, d7 or d21 of age and total RNA extraction.
  • Reverse transcription and real-time PCR were used to quantify mRNA abundance for: leptin, adiponectin, interleukin 1beta (IL-1beta), IL-6, IL-8, IL-10, IL-15, tumor necrosis factor alpha (TNFalpha), haptoglobin, vascular endothelial growth factor (VEGF), macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein 1 (MCP1) and cyclophilin.
  • Analysis of the mRNA abundance for these adipokines within adipose tissue from d1 to d21 of age demonstrated that neonatal development of adipokine expression varies among the different adipokines and the internal and external sites of adipose tissue deposition (PR versus SQ).
  • [MeSH-major] Adipokines / genetics. Adipose Tissue / chemistry

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  • (PMID = 18930835.001).
  • [ISSN] 1879-1107
  • [Journal-full-title] Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology
  • [ISO-abbreviation] Comp. Biochem. Physiol. B, Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adipokines; 0 / Haptoglobins; 0 / Interleukins; 0 / Lymphokines; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
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84. Langin D, Arner P: Importance of TNFalpha and neutral lipases in human adipose tissue lipolysis. Trends Endocrinol Metab; 2006 Oct;17(8):314-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Importance of TNFalpha and neutral lipases in human adipose tissue lipolysis.
  • The respective roles and regulation of hormone-sensitive lipase and adipose triglyceride lipase in spontaneous and hormone-stimulated lipolysis remain to be determined.
  • Tumor necrosis factor alpha stimulates triglyceride hydrolysis by multiple intracellular pathways acting on insulin signaling, G proteins and perilipins, and might contribute to enhanced plasma fatty acid levels in obesity.
  • Characterization of the lipolytic pathways might provide novel strategies to decrease free fatty acid production and reverse insulin resistance and other obesity-related metabolic complications.
  • [MeSH-major] Adipose Tissue / physiology. Lipase / physiology. Lipolysis / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 16938460.001).
  • [ISSN] 1043-2760
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; EC 3.1.1.3 / Lipase
  • [Number-of-references] 73
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85. Sashinami H, Nakane A: Adiponectin is required for enhancement of CCL2 expression in adipose tissue during Listeria monocytogenes infection. Cytokine; 2010 May;50(2):170-4
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  • [Title] Adiponectin is required for enhancement of CCL2 expression in adipose tissue during Listeria monocytogenes infection.
  • When leptin-deficient obese ob/ob mice were infected intraperitoneally with L. monocytogenes, the elimination of bacteria from spleen, liver, mesenteric lymph nodes and adipose tissue was inhibited in ob/ob mice compared with their heterozygote littermates, ob/?
  • mice. CCL2 expression in the adipose tissue of ob/?
  • Similarly, adiponectin expression was not observed in the adipose tissue of ob/ob mice.
  • [MeSH-major] Adiponectin / metabolism. Adipose Tissue / metabolism. Adipose Tissue / microbiology. Chemokine CCL2 / metabolism. Listeria monocytogenes / physiology. Listeriosis / metabolism
  • [MeSH-minor] Animals. Cell Line. Gene Expression Regulation. Immunity, Innate. Mice. Mice, Obese. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20045352.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / Tumor Necrosis Factor-alpha
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86. Eiras S, Teijeira-Fernández E, Salgado-Somoza A, Couso E, García-Caballero T, Sierra J, Juanatey JR: Relationship between epicardial adipose tissue adipocyte size and MCP-1 expression. Cytokine; 2010 Aug;51(2):207-12
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  • [Title] Relationship between epicardial adipose tissue adipocyte size and MCP-1 expression.
  • Epicardial adipose tissue (EAT) was discovered to play a key role in cardiovascular diseases by producing several inflammatory adipokines.
  • We sought to study whether EAT and subcutaneous adipose tissue (SAT) mean adipocyte sizes are related to the expression of adipokines in patients with cardiovascular diseases.
  • Monocyte chemoattractant protein (MCP)-1, interleukin (IL)-10 and tumor necrosis factor (TNF)-alpha were analyzed by real time RT-PCR, ELISA or immunohistochemistry.
  • These trends persisted after stratification for sex and coronary artery disease (CAD), but only the relationship between EAT MCP-1 and adipocyte size reached statistical significance in the larger group of men with CAD.
  • IL-10 and TNF-alpha expression were not associated to adipocyte size in EAT nor SAT.
  • [MeSH-minor] Aged. Cardiovascular Diseases / pathology. Cell Size. Coronary Artery Disease / metabolism. Coronary Artery Disease / pathology. Female. Gene Expression. Humans. Male. Middle Aged. Obesity / pathology

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20610178.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CCL2
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87. Højbjerre L, Rosenzweig M, Dela F, Bruun JM, Stallknecht B: Acute exercise increases adipose tissue interstitial adiponectin concentration in healthy overweight and lean subjects. Eur J Endocrinol; 2007 Nov;157(5):613-23
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  • [Title] Acute exercise increases adipose tissue interstitial adiponectin concentration in healthy overweight and lean subjects.
  • OBJECTIVE: We studied how an acute bout of exercise influences expression and concentration of adiponectin and regulators of adiponectin in adipose tissue and plasma.
  • DESIGN AND METHODS: Eight overweight and eight lean males were examined by large-pore microdialysis in s.c. abdominal adipose tissue (SCAAT) and had arterialized blood sampled.
  • RESULTS: Exercise increased the SCAAT interstitial adiponectin concentration in both overweight and lean subjects and concentrations did not differ between groups.
  • Plasma adiponectin did not increase during exercise and was similar in overweight and lean subjects.
  • Tumor necrosis factor- (TNF-) plasma concentration did not change during exercise in any of the groups, but SCAAT TNF- mRNA increased after exercise in both groups.
  • CONCLUSIONS: Acute exercise increases adipose tissue interstitial adiponectin concentration in both overweight and lean subjects with no major changes in plasma adiponectin concentration.

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  • (PMID = 17984241.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adiponectin
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88. Zhang Y, Bellows CF, Kolonin MG: Adipose tissue-derived progenitor cells and cancer. World J Stem Cells; 2010 Oct 26;2(5):103-13
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  • [Title] Adipose tissue-derived progenitor cells and cancer.
  • One of the factors complicating the clinical course of cancer is obesity, a progressively widespread medical condition resulting from overgrowth of white adipose tissue (WAT), commonly known as white fat.
  • The mechanisms by which obesity influences cancer risk and progression are not completely understood.
  • Cells of WAT secret soluble molecules (adipokines) that could stimulate tumor growth, although there is no consensus on which cell populations and which adipokines are important.
  • Recent reports suggest that WAT-derived mesenchymal stem (stromal) cells, termed adipose stem cells (ASC), may represent a cell population linking obesity and cancer.
  • Studies in animal models demonstrate that adipokines secreted by ASC can promote tumor growth by assisting in formation of new blood vessels, a process necessary for expansion of tumor mass.
  • Importantly, migration of ASC from WAT to tumors has been demonstrated, indicating that the tumor microenvironment in cancer may be modulated by ASC-derived trophic factors in a paracrine rather than in an endocrine manner.

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  • (PMID = 21607127.001).
  • [ISSN] 1948-0210
  • [Journal-full-title] World journal of stem cells
  • [ISO-abbreviation] World J Stem Cells
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA140388
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC3097931
  • [Keywords] NOTNLM ; Adipose tissue / Cancer / Cell mobilization / Obesity / Progenitor / Stromal / Tumor
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89. Bourlier V, Zakaroff-Girard A, Miranville A, De Barros S, Maumus M, Sengenes C, Galitzky J, Lafontan M, Karpe F, Frayn KN, Bouloumié A: Remodeling phenotype of human subcutaneous adipose tissue macrophages. Circulation; 2008 Feb 12;117(6):806-15
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  • [Title] Remodeling phenotype of human subcutaneous adipose tissue macrophages.
  • BACKGROUND: Adipose tissue macrophages (ATMs) have become a focus of attention recently because they have been shown to accumulate with an increase in fat mass and to be involved in the genesis of insulin resistance in obese mice.
  • ATMs isolated by an immunoselection protocol showed a mixed expression of proinflammatory (tumor necrosis factor-alpha, interleukin-6 [IL-6], IL-23, monocyte chemoattractant protein-1, IL-8, cyclooxygenase-2) and antiinflammatory (IL-10, transforming growth factor-beta, alternative macrophage activation-associated cc chemokine-1, cyclooxygenase-1) factors.

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  • (PMID = 18227385.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; EC 3.4.24.35 / Matrix Metalloproteinase 9
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90. Rosa Neto JC, Lira FS, Venancio DP, Cunha CA, Oyama LM, Pimentel GD, Tufik S, Oller do Nascimento CM, Santos RV, de Mello MT: Sleep deprivation affects inflammatory marker expression in adipose tissue. Lipids Health Dis; 2010;9:125
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sleep deprivation affects inflammatory marker expression in adipose tissue.
  • We investigated changes in the pro and anti-inflammatory cytokines and adipokines in different depots of white adipose tissue in rats.
  • Mesenteric (MEAT) and retroperitoneal (RPAT) adipose tissue, liver and serum were collected following completion of the PSD protocol.
  • Levels of interleukin (IL)-6, interleukin (IL)-10 and tumour necrosis factor (TNF)-α were analysed in MEAT and RPAT, and leptin, adiponectin, glucose, corticosterone and lipid profile levels were analysed in serum.
  • IL-10 protein concentration was not altered in either depot, and TNF-α levels decreased in MEAT.
  • Glucose, triglycerides (TG), VLDL and leptin decreased in serum after 96 hours of PSD; adiponectin was not altered and corticosterone was increased.
  • CONCLUSION: PSD decreased fat mass and may modulate the cytokine content in different depots of adipose tissue.
  • The inflammatory response was diminished in both depots of adipose tissue, with increased IL-6 levels in RPAT and decreased TNF-α protein concentrations in MEAT and increased levels of corticosterone in serum.
  • [MeSH-major] Adipose Tissue / metabolism. Inflammation / blood. Sleep Deprivation / blood. Sleep Deprivation / physiopathology
  • [MeSH-minor] Adipokines / blood. Animals. Corticosterone / blood. Interleukin-10 / blood. Interleukin-6 / blood. Leptin / blood. Male. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 21034496.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adipokines; 0 / Interleukin-6; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; W980KJ009P / Corticosterone
  • [Other-IDs] NLM/ PMC2987991
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91. Lee MJ, Kim J, Kim MY, Bae YS, Ryu SH, Lee TG, Kim JH: Proteomic analysis of tumor necrosis factor-alpha-induced secretome of human adipose tissue-derived mesenchymal stem cells. J Proteome Res; 2010 Apr 5;9(4):1754-62
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  • [Title] Proteomic analysis of tumor necrosis factor-alpha-induced secretome of human adipose tissue-derived mesenchymal stem cells.
  • Human adipose tissue-derived mesenchymal stem cells (hASCs) are useful for regeneration of inflamed or injured tissues.
  • To identify secreted hASC proteins during inflammation, hASCs were exposed to tumor necrosis factor-alpha (TNF-alpha) and conditioned media derived from hASCs were analyzed by liquid chromatography coupled with tandem mass spectrometry.
  • [MeSH-major] Adipose Tissue / cytology. Mesenchymal Stromal Cells / metabolism. Proteome / drug effects. Proteomics / methods. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 20184379.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Proteome; 0 / Tumor Necrosis Factor-alpha; EC 3.4.- / Cathepsins; EC 3.4.24.7 / MMP1 protein, human; EC 3.4.24.7 / Matrix Metalloproteinase 1
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92. Poglio S, Galvani S, Bour S, André M, Prunet-Marcassus B, Pénicaud L, Casteilla L, Cousin B: Adipose tissue sensitivity to radiation exposure. Am J Pathol; 2009 Jan;174(1):44-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose tissue sensitivity to radiation exposure.
  • Treatment of cancer using radiation can be significantly compromised by the development of severe acute and late damage to normal tissue.
  • Treatments that either reduce the risk and severity of damage or that facilitate the healing of radiation injuries are being developed, including autologous adipose tissue grafts to repair tissue defects or involutional disorders that result from tumor resection.
  • Adipose tissue is specialized in energy storage and contains different cell types, including preadipocytes, which could be used for autologous transplantation.
  • It has long been considered a poorly proliferative connective tissue; however, the acute effects of ionizing radiation on adipose tissue have not been investigated.
  • Therefore, the aim of this study was to characterize the alterations induced in adipose tissue by total body irradiation.
  • Decreases in the proliferation and differentiation capacities of non-hematopoietic progenitors were also observed following irradiation.
  • Together, these data demonstrate that subcutaneous adipose tissue is very sensitive to irradiation, leading to a profound alteration of its developmental potential.
  • This damage could also alter the reconstructive properties of adipose tissue and, therefore, calls into question its use in autologous fat transfer following radiotherapy.
  • [MeSH-major] Adipocytes / radiation effects. Adipose Tissue / radiation effects. Cell Differentiation / radiation effects. Cell Proliferation / radiation effects. Radiation Injuries, Experimental / pathology

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  • (PMID = 19095959.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2631317
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93. Duque-Guimarães DE, de Castro J, Martinez-Botas J, Sardinha FL, Ramos MP, Herrera E, do Carmo Md: Early and prolonged intake of partially hydrogenated fat alters the expression of genes in rat adipose tissue. Nutrition; 2009 Jul-Aug;25(7-8):782-9
Hazardous Substances Data Bank. Soybean oil .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Early and prolonged intake of partially hydrogenated fat alters the expression of genes in rat adipose tissue.
  • OBJECTIVE: Our previous study indicated that partially hydrogenated fat (PHF) diets, rich in trans-isomers, alter plasma lipids and increase the lipogenesis rate on adipose tissue in rats at a young age.
  • In the present study we investigated the effects of dietary PHF on the expression of genes associated with glucose and lipid metabolism in rat adipose tissue.
  • METHODS: Female Wistar rats were fed normolipidic diets containing PHF (rich in trans-fatty acids and poor in polyunsaturated fatty acids [PUFAs]), soy oil (rich in omega-6 PUFAs), and fish oil (rich in omega-3 PUFAs) during gestation and lactation; young male pups were fed the same diets from weaning until 120 d of life.
  • The mRNA expression of peroxisome proliferator-activated receptor-gamma, tumor necrosis factor-alpha, resistin, adiponectin, and leptin were analyzed in retroperitoneal adipose tissue (RET) using real time polymerase chain reaction.
  • The RET of PHF incorporated trans-fatty acids, whereas fish oil and soy oil groups had increased omega-3 and omega-6 PUFAs, respectively.
  • In the RET the PHF group had the highest resistin and tumor necrosis factor-alpha levels and the lowest adiponectin and peroxisome proliferator-activated receptor-gamma gene expressions, whereas the fish oil group had the highest peroxisome proliferator-activated receptor-gamma and the lowest leptin gene expression.
  • These changes may be an effect of the smaller proportions of PUFAs in this fat, instead of being only caused by trans-fatty acids.
  • [MeSH-major] Adipokines / metabolism. Dietary Fats / pharmacology. Fatty Acids, Unsaturated / pharmacology. Gene Expression / drug effects. Intra-Abdominal Fat / drug effects
  • [MeSH-minor] Animals. Blood Glucose. Body Weight / drug effects. Female. Fish Oils / pharmacology. Hydrogenation. Insulin / blood. Male. Organ Size / drug effects. PPAR gamma / genetics. PPAR gamma / metabolism. Pregnancy. RNA, Messenger / metabolism. Rats. Rats, Wistar. Soybean Oil / pharmacology. Triglycerides / blood. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19251397.001).
  • [ISSN] 1873-1244
  • [Journal-full-title] Nutrition (Burbank, Los Angeles County, Calif.)
  • [ISO-abbreviation] Nutrition
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / Blood Glucose; 0 / Dietary Fats; 0 / Fatty Acids, Unsaturated; 0 / Fish Oils; 0 / Insulin; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 8001-22-7 / Soybean Oil
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94. Wu ZH, Zhao SP, Chu LX, Ye HJ: Pioglitazone reduces tumor necrosis factor-alpha serum concentration and mRNA expression of adipose tissue in hypercholesterolemic rabbits. Int J Cardiol; 2010 Jan 21;138(2):151-6
Hazardous Substances Data Bank. PIOGLITAZONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pioglitazone reduces tumor necrosis factor-alpha serum concentration and mRNA expression of adipose tissue in hypercholesterolemic rabbits.
  • BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is an inflammatory cytokine involved in atherogenesis.
  • Adipose tissue is an important source of endogenous TNF-alpha production.
  • Pioglitazone, a member of the thiazolidinediones (TZDs), has anti-inflammatory and anti-atherogenic properties, while underlying mechanism has not been fully elucidated.
  • The aim of this study was to evaluate the effect of pioglitazone on TNF-alpha serum concentration and mRNA expressions of subcutaneous adipose tissue in hypercholesterolemic rabbits.
  • Subcutaneous adipose tissue was collected for RNA analysis.
  • RT-PCR was used to evaluate TNF-alpha mRNA expressions in adipose tissue and adipocytes.
  • Though having no effect on serum glucose level and lipid profile, pioglitazone administration significantly reduced circulating TNF-alpha concentrations, which were positively correlated with TNF-alpha mRNA expressions of adipose tissue (r=0.53, P<0.01).
  • [MeSH-major] Hypercholesterolemia / drug therapy. Hypoglycemic Agents / pharmacology. Subcutaneous Fat / physiology. Thiazolidinediones / pharmacology. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / genetics

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  • [Copyright] Copyright (c) 2008 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 18809217.001).
  • [ISSN] 1874-1754
  • [Journal-full-title] International journal of cardiology
  • [ISO-abbreviation] Int. J. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Cholesterol, Dietary; 0 / Cholesterol, LDL; 0 / Hypoglycemic Agents; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Thiazolidinediones; 0 / Tumor Necrosis Factor-alpha; X4OV71U42S / pioglitazone
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95. Dali-Youcef N, Mataki C, Coste A, Messaddeq N, Giroud S, Blanc S, Koehl C, Champy MF, Chambon P, Fajas L, Metzger D, Schoonjans K, Auwerx J: Adipose tissue-specific inactivation of the retinoblastoma protein protects against diabesity because of increased energy expenditure. Proc Natl Acad Sci U S A; 2007 Jun 19;104(25):10703-8
The Lens. Cited by Patents in .

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  • [Title] Adipose tissue-specific inactivation of the retinoblastoma protein protects against diabesity because of increased energy expenditure.
  • The role of the tumor suppressor retinoblastoma protein (pRb) has been firmly established in the control of cell cycle, apoptosis, and differentiation.
  • Recently, it was demonstrated that lack of pRb promotes a switch from white to brown adipocyte differentiation in vitro.
  • We used the Cre-Lox system to specifically inactivate pRb in adult adipose tissue.
  • Moreover, pRb(-/-) mouse embryonic fibroblasts displayed higher proliferation and apoptosis rates than pRb(+/+) mouse embryonic fibroblasts, which could contribute to the altered white adipose tissue morphology.
  • Taken together, our data support a direct role of pRb in adipocyte cell fate determination in vivo and suggest that pRb could serve as a potential therapeutic target to trigger mitochondrial activation in white adipose tissue and brown adipose tissue, favoring an increase in energy expenditure and subsequent weight loss.
  • [MeSH-major] Adipose Tissue, Brown / physiology. Adipose Tissue, White / physiology. Energy Metabolism. Obesity / prevention & control. Retinoblastoma Protein / physiology

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  • (PMID = 17556545.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Mitochondrial; 0 / Dietary Fats; 0 / Retinoblastoma Protein
  • [Other-IDs] NLM/ PMC1965576
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96. Garg A: Adipose tissue dysfunction in obesity and lipodystrophy. Clin Cornerstone; 2006;8 Suppl 4:S7-S13
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  • [Title] Adipose tissue dysfunction in obesity and lipodystrophy.
  • The primary function of adipose tissue is to store energy in the form of triglycerides during periods of energy excess and to release the energy during fasting or starvation as free fatty acids and glycerol.
  • Adipose tissue secretes a variety of peptides called adipocytokines (eg, leptin, adiponectin, tumor necrosis factor-alpha, interleukin-6, resistin, visfatin) that have endocrine, autocrine, and paracrine effects on the brain, liver, and skeletal muscles.
  • Adipose tissue also aromatizes androgens to estrogens, and some adipose tissue depots (mechanical fat) serve a protective or cushioning function.
  • Dysfunction of adipose tissue can result in insulin resistance and its metabolic complications in patients with excess body fat (obesity) or markedly reduced body fat (lipodystrophy).
  • Alterations in free fatty acid and adipocytokine release from adipose tissue may underlie metabolic complications.
  • [MeSH-major] Adipose Tissue / metabolism. Cytokines / biosynthesis. Lipodystrophy / etiology. Obesity / metabolism. Triglycerides / metabolism

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  • (PMID = 17208666.001).
  • [ISSN] 1098-3597
  • [Journal-full-title] Clinical cornerstone
  • [ISO-abbreviation] Clin Cornerstone
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Triglycerides
  • [Number-of-references] 33
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97. Fujisaka S, Usui I, Bukhari A, Ikutani M, Oya T, Kanatani Y, Tsuneyama K, Nagai Y, Takatsu K, Urakaze M, Kobayashi M, Tobe K: Regulatory mechanisms for adipose tissue M1 and M2 macrophages in diet-induced obese mice. Diabetes; 2009 Nov;58(11):2574-82
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  • [Title] Regulatory mechanisms for adipose tissue M1 and M2 macrophages in diet-induced obese mice.
  • OBJECTIVE: To characterize the phenotypic changes of adipose tissue macrophages (ATMs) under different conditions of insulin sensitivity.
  • RESEARCH DESIGN AND METHODS: The number and the expressions of marker genes for M1 and M2 macrophages from mouse epididymal fat tissue were analyzed using flow cytometry after the mice had been subjected to a high-fat diet (HFD) and pioglitazone treatment.
  • RESULTS: Most of the CD11c-positive M1 macrophages and the CD206-positive M2 macrophages in the epididymal fat tissue were clearly separated using flow cytometry.
  • Not only the numbers of M1 ATMs and the expression of M1 marker genes, such as tumor necrosis factor-alpha and monocyte chemoattractant protein-1, but also the M1-to-M2 ratio were increased by an HFD and decreased by subsequent pioglitazone treatment, suggesting the correlation with whole-body insulin sensitivity.
  • We also found that the increased number of M2 ATMs after an HFD was associated with the upregulated expression of interleukin (IL)-10, an anti-inflammatory Th2 cytokine, in the adipocyte fraction as well as in adipose tissue.
  • The systemic overexpression of IL-10 by an adenovirus vector increased the expression of M2 markers in adipose tissue.
  • [MeSH-major] Adipose Tissue / physiology. Macrophages / physiology. Obesity / physiopathology

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  • (PMID = 19690061.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Hypoglycemic Agents; 0 / Thiazolidinediones; 130068-27-8 / Interleukin-10; 63231-63-0 / RNA; X4OV71U42S / pioglitazone
  • [Other-IDs] NLM/ PMC2768159
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98. Fang B, Luo S, Song Y, Li N, Cao Y: Hemangioblastic characteristics of human adipose tissue-derived adult stem cells in vivo. Arch Med Res; 2009 May;40(4):311-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemangioblastic characteristics of human adipose tissue-derived adult stem cells in vivo.
  • Recent studies have demonstrated the existence of a population of adipose tissue-derived adult stem (ADAS) cells that can undergo multilineage differentiation in vitro.
  • [MeSH-major] Adipose Tissue / physiology. Adult Stem Cells / physiology. Hemangioblasts / physiology
  • [MeSH-minor] Adult. Animals. Cell Differentiation / physiology. Hematopoietic Stem Cell Transplantation. Humans. Male. Mice. Mice, SCID. Neovascularization, Physiologic

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  • (PMID = 19608022.001).
  • [ISSN] 1873-5487
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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99. Baranova A, Schlauch K, Elariny H, Jarrar M, Bennett C, Nugent C, Gowder SJ, Younoszai Z, Collantes R, Chandhoke V, Younossi ZM: Gene expression patterns in hepatic tissue and visceral adipose tissue of patients with non-alcoholic fatty liver disease. Obes Surg; 2007 Aug;17(8):1111-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression patterns in hepatic tissue and visceral adipose tissue of patients with non-alcoholic fatty liver disease.
  • BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) and its progressive form, non-alcoholic steatohepatitis (NASH), are among the least understood metabolic consequences of obesity.
  • Increasingly, omental adipose tissue is recognized as a biologically active organ in the pathogenesis of NAFLD.
  • Differences in transcriptional regulation in omental adipose tissue and liver tissue may provide important insights into the pathogenesis of NAFLD and its progression.
  • METHODS: Transcriptional profiles were obtained for liver and visceral adipose specimens of morbidly obese patients undergoing bariatric surgery.
  • RESULTS: Tissue from patients with NASH showed prominent adipose-specific deregulation of genes related to inflammation and the immune system.
  • A number of liver and adipose-specific functional networks, including those centered at TNFalpha, JUN/JUNB, and IFNgamma were highlighted as related to the NASH pathogenesis.
  • [MeSH-major] Adipocytes / physiology. Fatty Liver / genetics. Gene Expression Profiling. Gene Expression Regulation / physiology. Intra-Abdominal Fat / cytology. Liver / physiology
  • [MeSH-minor] Adult. Enzyme-Linked Immunosorbent Assay. Female. Genes, jun / genetics. Humans. Interferon-gamma / genetics. Interferon-gamma / physiology. Interleukin-6 / blood. Leptin / metabolism. Male. Middle Aged. Obesity / genetics. Obesity / metabolism. Protein Array Analysis. Tumor Necrosis Factor-alpha / blood


100. Wandler A, Bruun JM, Nielsen MP, Richelsen B: Ethanol exerts anti-inflammatory effects in human adipose tissue in vitro. Mol Cell Endocrinol; 2008 Dec 16;296(1-2):26-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ethanol exerts anti-inflammatory effects in human adipose tissue in vitro.
  • Human adipose tissue (AT) and obesity is characterised by low-grade inflammation, so the present study wanted to investigate the effects of ethanol on inflammation in human AT in vitro.
  • Ethanol decreased CD68 mRNA (p<0.001), which correlated with the investigated adipokines (p<0.05) but not adiponectin (p>0.05).
  • [MeSH-major] Adipose Tissue / drug effects. Adipose Tissue / pathology. Anti-Inflammatory Agents / pharmacology. Ethanol / pharmacology. Inflammation / prevention & control
  • [MeSH-minor] Adipokines / pharmacology. Adiponectin / genetics. Adiponectin / metabolism. Adult. Antigens, CD / genetics. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / genetics. Antigens, Differentiation, Myelomonocytic / metabolism. Cells, Cultured. Chemokine CCL2 / genetics. Chemokine CCL2 / metabolism. Drug Evaluation, Preclinical. Female. Humans. Interleukin-6 / genetics. Interleukin-6 / metabolism. Interleukin-8 / genetics. Interleukin-8 / metabolism. Lipopolysaccharides / pharmacology. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18840498.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / ADIPOQ protein, human; 0 / Adipokines; 0 / Adiponectin; 0 / Anti-Inflammatory Agents; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CCL2 protein, human; 0 / CD68 antigen, human; 0 / Chemokine CCL2; 0 / IL6 protein, human; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 3K9958V90M / Ethanol
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