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6. Brand MD, Parker N, Affourtit C, Mookerjee SA, Azzu V: Mitochondrial uncoupling protein 2 in pancreatic β-cells. Diabetes Obes Metab; 2010 Oct;12 Suppl 2:134-40
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  • [Title] Mitochondrial uncoupling protein 2 in pancreatic β-cells.
  • Pancreatic β-cells have remarkable bioenergetics in which increased glucose supply upregulates the cytosolic ATP/ADP ratio and increases insulin secretion.
  • This arrangement allows glucose-stimulated insulin secretion (GSIS) to be regulated by the coupling efficiency of oxidative phosphorylation.
  • Importantly, however, the enhancement of GSIS is robustly recapitulated with acute UCP2 knockdown in INS-1E insulinoma cells.
  • UCP2 protein level in these cells is dynamically regulated, over at least a fourfold concentration range, by rapid proteolysis (half-life less than 1 h) opposing regulated gene transcription and mRNA translation.
  • Evidence for proteasomal turnover of UCP2 includes sensitivity of degradation to classic proteasome inhibitors in cells, and reconstitution of degradation in vitro in mitochondria incubated with ubiquitin and the cytosolic 26S proteasome.
  • These dynamic changes in UCP2 content may provide a fine level of control over GSIS in β-cells.
  • [MeSH-major] Energy Metabolism / physiology. Insulin / secretion. Insulin-Secreting Cells / metabolism. Ion Channels / physiology. Mitochondrial Proteins / physiology

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 21029310.001).
  • [ISSN] 1463-1326
  • [Journal-full-title] Diabetes, obesity & metabolism
  • [ISO-abbreviation] Diabetes Obes Metab
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / P01AG025901; United States / NIA NIH HHS / AG / P30 AG025708; United States / NIA NIH HHS / AG / PL1AG032118; United States / NIA NIH HHS / AG / R01 AG033542; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin; 0 / Ion Channels; 0 / Mitochondrial Proteins; 0 / Reactive Oxygen Species; 0 / mitochondrial uncoupling protein 2; IY9XDZ35W2 / Glucose
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7. d'Annunzio G, Giannattasio A, Poggi E, Castellano E, Calvi A, Pistorio A, Barabino A, Lorini R: Beta-cell autoimmunity in pediatric celiac disease: the case for routine screening? Diabetes Care; 2009 Feb;32(2):254-6
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  • [Title] Beta-cell autoimmunity in pediatric celiac disease: the case for routine screening?
  • OBJECTIVE: To evaluate the prevalence of beta-cell autoimmunity and the usefulness of a type 1 diabetes screening in patients with celiac disease.
  • RESEARCH DESIGN AND METHODS: We measured GAD antibodies (GADAs), insulinoma-associated protein 2 antigens (IA-2As), and insulin autoantibodies (IAAs) in 188 young Italian patients with celiac disease (66 male [35.1%]).
  • Mean age at celiac disease diagnosis was 5.4 years (0.5-17.1), and mean celiac disease duration was 4.2 years (0-28.8).
  • Celiac disease was diagnosed by jejunal biopsy after positivity for endomysial and tissue transglutaminase antibody was confirmed.
  • There was no significant association among beta-cell autoimmunity and sex, age, pubertal stage, family history, or coexistence of other autoimmune disorders; compliance to a gluten-free diet was confirmed.
  • CONCLUSIONS: Our results showed a low prevalence of beta-cell autoimmunity and do not support a precocious screening for beta-cell autoimmunity in young celiac disease patients.
  • [MeSH-major] Autoimmune Diseases / epidemiology. Celiac Disease / immunology. Insulin-Secreting Cells / immunology
  • [MeSH-minor] Adolescent. Age of Onset. Autoantibodies / blood. Autoimmunity. Child. Child, Preschool. Female. Humans. Infant. Insulin Antibodies / blood. Italy. Male

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  • (PMID = 19017767.001).
  • [ISSN] 1935-5548
  • [Journal-full-title] Diabetes care
  • [ISO-abbreviation] Diabetes Care
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / ICA512 autoantibody; 0 / Insulin Antibodies
  • [Other-IDs] NLM/ PMC2628689
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8. Tomita T: Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors. Pancreas; 2007 Nov;35(4):e18-22
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  • [Title] Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors.
  • OBJECTIVES: Immunocytochemical staining for lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) is able to recognize lymphatic vessel endothelium and pancreatic endocrine cells (PETs).
  • Pancreatic endocrine tumors were studied for LYVE-1 immunocytochemical staining compared with normal pancreatic islets to detect possible presence of LYVE-1 in PETs.
  • METHODS: Twenty-five cases of primary and metastatic PETs were immunocytochemically stained for LYVE-1, including insulinomas, glucagonomas, somatostatinoma, pancreatic polypeptidomas, gastrinomas, and nonfunctioning tumors.
  • RESULTS: All normal pancreatic islet cells were positive for LYVE-1, whereas 2 cases of 25 PETs, 1 each of gastrinoma and nonfunctioning tumor, were positive for LYVE-1, retaining immunocytochemical reactivity of islet cells.
  • CONCLUSIONS: Normal pancreatic islets were positive for LYVE-1, whereas only 2 of 25 PETs were positive, suggesting that most PETs lost LYVE-1 or contained below detectable levels of LYVE-1.
  • The presence of LYVE-1 in pancreatic islets and in some PETs may suggest structure-function relationship of LYVE-1/lymphatic vessel in hormone synthesis and secretion.
  • [MeSH-major] Gastrinoma / chemistry. Glucagonoma / chemistry. Immunohistochemistry. Insulinoma / chemistry. Islets of Langerhans / chemistry. Pancreatic Neoplasms / chemistry. Somatostatinoma / chemistry. Vesicular Transport Proteins / analysis

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  • (PMID = 18090227.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LYVE1 protein, human; 0 / Vesicular Transport Proteins
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9. Jasinski JM, Eisenbarth GS: Insulin as a primary autoantigen for type 1A diabetes. Clin Dev Immunol; 2005 Sep;12(3):181-6
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  • [Title] Insulin as a primary autoantigen for type 1A diabetes.
  • Type 1A diabetes mellitus is caused by specific and progressive autoimmune destruction of the beta cells in the islets of Langerhans whereas the other cell types in the islet (alpha, delta, and PP) are spared.
  • The autoantigens of Type 1A diabetes may be divided into subgroups based on their tissue distributions: Beta-cell-specific antigens like insulin, insulin derivatives, and IGRP (Islet-specific Glucose-6-phosphatase catalytic subunit Related Peptide); neurendocrine antigens such as carboxypeptidase H, insulinoma-associated antigen (IA-2), glutamic acid decarboxylase (GAD65), and carboxypeptidase E; and those expressed ubiquitously like heat shock protein 60 (a putative autoantigen for type 1 diabetes).
  • This review will focus specifically on insulin as a primary autoantigen, an essential target for disease, in type 1A diabetes mellitus.
  • In particular, immunization with insulin peptide B:9-23 can be used to induce insulin autoantibodies and diabetes in animal models or used to prevent diabetes.
  • Genetic manipulation of the insulin 1 and 2 genes reciprocally alters development of diabetes in the NOD mouse, and insulin gene polymorphisms are important determinants of childhood diabetes.
  • We are pursuing the hypothesis that insulin is a primary autoantigen for type 1 diabetes, and thus the pathogenesis of the disease relates to specific recognition of one or more peptides.

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  • (PMID = 16295523.001).
  • [ISSN] 1740-2522
  • [Journal-full-title] Clinical & developmental immunology
  • [ISO-abbreviation] Clin. Dev. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI95380; United States / NIDDK NIH HHS / DK / DK32493; United States / NIDDK NIH HHS / DK / DK32083; United States / NIDDK NIH HHS / DK / DK50970; United States / NCRR NIH HHS / RR / M01 RR00051; United States / NIDDK NIH HHS / DK / DK55969; United States / NIDDK NIH HHS / DK / P30 DK57516; United States / NIDDK NIH HHS / DK / DK62718; United States / NIAID NIH HHS / AI / AI46374; United States / NCRR NIH HHS / RR / M01 RR00069; United States / NIAID NIH HHS / AI / AI39213; United States / NIAID NIH HHS / AI / AI50864
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Autoantigens; 0 / Epitopes; 0 / Insulin; 0 / Protein Precursors; 61116-24-3 / preproinsulin; 9035-68-1 / Proinsulin
  • [Number-of-references] 58
  • [Other-IDs] NLM/ PMC2275421
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10. Fukazawa K, Kayanuma H, Kanai E, Sakata M, Shida T, Suganuma T: Insulinoma with basal ganglion involvement detected by magnetic resonance imaging in a dog. J Vet Med Sci; 2009 May;71(5):689-92
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  • [Title] Insulinoma with basal ganglion involvement detected by magnetic resonance imaging in a dog.
  • Suspecting a metabolic disorder, an abdominal ultrasonography was performed, and a tumor was found in the pancreas.
  • The pancreatic tumor was surgically removed based on suspicion that it had induced the brain damage.
  • The resected tumor was histopathologically diagnosed as an insulinoma.
  • Consequently, the tumor was thought to have induced the lesion in the basal ganglion, and this was verified by MRI.

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  • (PMID = 19498303.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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11. L'Amoreaux WJ, Cuttitta C, Santora A, Blaize JF, Tachjadi J, El Idrissi A: Taurine regulates insulin release from pancreatic beta cell lines. J Biomed Sci; 2010;17 Suppl 1:S11
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  • [Title] Taurine regulates insulin release from pancreatic beta cell lines.
  • BACKGROUND: Pancreatic beta-cells release insulin via an electrogenic response triggered by an increase in plasma glucose concentrations.
  • The critical plasma glucose concentration has been determined to be approximately 3 mM, at which time both insulin and GABA are released from pancreatic beta-cells.
  • Taurine, a beta-sulfonic acid, may be transported into cells to balance osmotic pressure.
  • The taurine transporter (TauT) has been described in pancreatic tissue, but the function of taurine in insulin release has not been established.
  • Uptake of taurine by pancreatic beta-cells may alter membrane potential and have an effect on ion currents.
  • If taurine uptake does alter beta-cell current, it might have an effect on exocytosis of cytoplasmic vesicle.
  • We wished to test the effect of taurine on regulating release of insulin from the pancreatic beta-cell.
  • METHODS: Pancreatic beta-cell lines Hit-TI5 (Syrian hamster) and Rin-m (rat insulinoma) were used in these studies.
  • Cells were grown to an 80% confluence on uncoated cover glass in RPMI media containing 10% fetal horse serum.
  • The cells were then adapted to a serum-free, glucose free environment for 24 hours.
  • At that time, the cells were treated with either 1 mM glucose, 1 mM taurine, 1 mM glucose + 1 mM taurine, 3 mM glucose, or 3 mM glucose + 1 mM taurine.
  • The cells were examined by confocal microscopy for cytoplasmic levels of insulin.
  • RESULTS: In both cell lines, 1 mM glucose had no effect on insulin levels and served as a control.
  • Cells starved of glucose had a significant reduction (p<0.001) in the level of insulin, but this level was significantly higher than all other treatments.
  • As expected, the 3 mM glucose treatment resulted in a statistically lower (p<0.001) insulin level than control cells.
  • Interestingly, 1 mM taurine also resulted in a statistically lower level of insulin (p<0.001) compared to controls when either no glucose or 1 mM glucose was present.
  • Cells treated with 1 mM taurine plus 3 mM glucose showed a level of insulin similar to that of 3 mM glucose alone.
  • CONCLUSIONS: Taurine administration can alter the electrogenic response in beta-cell lines, leading to a change in calcium homeostasis and a subsequent decrease in intracellular insulin levels.
  • The consequence of these actions could represent a method of increasing plasma insulin levels leading to a decrease in plasma glucose levels.
  • [MeSH-major] Insulin / secretion. Insulin-Secreting Cells. Taurine / pharmacology
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Line. Cricetinae. Glucose / pharmacology. Membrane Glycoproteins / metabolism. Membrane Transport Proteins / metabolism. Rats. gamma-Aminobutyric Acid / metabolism

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  • (PMID = 20804585.001).
  • [ISSN] 1423-0127
  • [Journal-full-title] Journal of biomedical science
  • [ISO-abbreviation] J. Biomed. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Membrane Glycoproteins; 0 / Membrane Transport Proteins; 148686-53-7 / taurine transporter; 1EQV5MLY3D / Taurine; 56-12-2 / gamma-Aminobutyric Acid; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2994409
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12. Mziaut H, Kersting S, Knoch KP, Fan WH, Trajkovski M, Erdmann K, Bergert H, Ehehalt F, Saeger HD, Solimena M: ICA512 signaling enhances pancreatic beta-cell proliferation by regulating cyclins D through STATs. Proc Natl Acad Sci U S A; 2008 Jan 15;105(2):674-9
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  • [Title] ICA512 signaling enhances pancreatic beta-cell proliferation by regulating cyclins D through STATs.
  • Changes in metabolic demands dynamically regulate the total mass of adult pancreatic beta-cells to adjust insulin secretion and preserve glucose homeostasis.
  • Glucose itself is a major regulator of beta-cell proliferation by inducing insulin secretion and activating beta-cell insulin receptors.
  • Here, we show that islet cell autoantigen 512 (ICA512)/IA-2, an intrinsic tyrosine phosphatase-like protein of the secretory granules, activates a complementary pathway for beta-cell proliferation.
  • On granule exocytosis, the ICA512 cytoplasmic domain is cleaved and the resulting cytosolic fragment (ICA512-CCF) moves into the nucleus where it enhances the levels of phosphorylated STAT5 and STAT3, thereby inducing insulin gene transcription and granule biogenesis.
  • We now show that knockdown of ICA512 decreases cyclin D1 levels and proliferation of insulinoma INS-1 cells, whereas beta-cell regeneration is reduced in partially pancreatectomized ICA512-/- mice.
  • Conversely, overexpression of ICA512-CCF increases both cyclin D1 and D2 levels and INS-1 cell proliferation.
  • Up-regulation of cyclin D1 and D2 by ICA512-CCF is affected by knockdown of STAT3 and STAT5, respectively, whereas it does not require insulin signaling.
  • These results identify ICA512 as a regulator of cyclins D and beta-cell proliferation through STATs and may have implication for diabetes therapy.
  • [MeSH-major] Cyclins / biosynthesis. Gene Expression Regulation. Insulin-Secreting Cells / metabolism. Receptor-Like Protein Tyrosine Phosphatases, Class 8 / physiology. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Cyclin D. Cyclin D2. Diabetes Mellitus / drug therapy. Diabetes Mellitus / metabolism. Humans. Insulin / metabolism. Models, Biological. Phosphorylation. Rats. Regeneration. Signal Transduction


13. Leow MK, Wyckoff J: Under-recognised paradox of neuropathy from rapid glycaemic control. Postgrad Med J; 2005 Feb;81(952):103-7
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  • Insulin induced neuropathy has been reported previously in people with diabetes treated with insulin, and subsequently reported in patients with insulinomas.
  • [MeSH-major] Diabetic Neuropathies / chemically induced. Hemoglobin A, Glycosylated / drug effects. Hyperglycemia / drug therapy. Hypoglycemia / chemically induced. Hypoglycemic Agents / adverse effects. Insulin / adverse effects

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  • (PMID = 15701742.001).
  • [ISSN] 0032-5473
  • [Journal-full-title] Postgraduate medical journal
  • [ISO-abbreviation] Postgrad Med J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Hemoglobin A, Glycosylated; 0 / Hypoglycemic Agents; 0 / Insulin
  • [Number-of-references] 38
  • [Other-IDs] NLM/ PMC1743196
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4. Jürgensen C, Schuppan D, Neser F, Ernstberger J, Junghans U, Stölzel U: EUS-guided alcohol ablation of an insulinoma. Gastrointest Endosc; 2006 Jun;63(7):1059-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EUS-guided alcohol ablation of an insulinoma.
  • BACKGROUND: Surgical resection is currently considered to be the criterion standard for treatment of insulinomas.
  • EUS-guided ethanol ablation of endocrine tumors has not been reported before.
  • INTERVENTION: A 78-year-old woman was referred with typical symptoms of an insulinoma.
  • Because of severe complications during several hypoglycemic episodes, a poor general condition, and strict refusal of surgical resection, the decision was made to ablate the insulinoma by EUS-guided alcohol injection.
  • A total of 8 mL 95% ethanol was injected into the tumor.
  • Based on clinical, morphologic, and biochemical criteria, we achieved a durable complete remission of the tumor.
  • CONCLUSIONS: EUS-guided ablation may become a minimally invasive alternative for patients with insulinomas in whom surgery is not feasible.
  • [MeSH-major] Endosonography. Ethanol / administration & dosage. Insulinoma / drug therapy. Pancreatic Neoplasms / drug therapy

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  • (PMID = 16733126.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 3K9958V90M / Ethanol
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15. Fontanière S, Casse H, Bertolino P, Zhang CX: Analysis of p27(Kip1) expression in insulinomas developed in pancreatic beta-cell specific Men1 mutant mice. Fam Cancer; 2006;5(1):49-54
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  • [Title] Analysis of p27(Kip1) expression in insulinomas developed in pancreatic beta-cell specific Men1 mutant mice.
  • Multiple Endocrine Neoplasia type 1 (MEN1) is a hereditary disease characterised by the occurrence of multiple endocrine tumours.
  • Interestingly, it has been recently reported that p27(Kip1) expression is regulated by menin and that decreased p27(Kip1) expression can be found in MEN1 insulinomas and parathyroid adenomas.
  • In order to address whether and when p27(Kip1) expression alters during insulinoma development in pancreatic beta-cell-specific Men1 mutant mice, we analysed p27(Kip1) expression in islet lesions from mutant mice at different ages.
  • Our data revealed that p27(Kip1) protein expression was reduced in 40 out of 52 (77%) insulinomas analysed, whereas the remaining 12 insulinomas (23%) did not show altered p27(Kip1) expression.
  • No difference between the insulinomas with and without decreased p27(Kip1) expression could be observed in terms of histological features or menin inactivation.
  • Furthermore, our analysis on hyperplastic and dysplastic islets developed in young mutant mice showed the lack of detectable alteration in p27(Kip1) expression, despite evident loss of menin expression in a substantial proportion of islet cells.
  • Our work confirms the altered p27(Kip1) expression reported in tumours from MEN1 patients, whereas it suggests that other molecular events may also participate in the tumorigenesis process initiated by the Men1 gene inactivation.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p27 / genetics. Gene Expression Regulation, Neoplastic. Insulinoma / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cell Survival. Disease Models, Animal. Down-Regulation. Gene Deletion. Immunohistochemistry. Islets of Langerhans / cytology. Mice. Mice, Mutant Strains. Probability. Proto-Oncogene Proteins / genetics. Sensitivity and Specificity. Tumor Cells, Cultured


16. Vezzosi D, Bennet A, Fauvel J, Caron P: Insulin, C-peptide and proinsulin for the biochemical diagnosis of hypoglycaemia related to endogenous hyperinsulinism. Eur J Endocrinol; 2007 Jul;157(1):75-83
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  • [Title] Insulin, C-peptide and proinsulin for the biochemical diagnosis of hypoglycaemia related to endogenous hyperinsulinism.
  • OBJECTIVE: We evaluated the respective value of insulin, C-peptide and proinsulin levels in 33 patients with endogenous hyperinsulinism and in 67 controls to determine the best parameters and thresholds to make or to rule out the diagnosis of endogenous hyperinsulinism.
  • RESULTS: When blood glucose levels were below 2.5 mmol/l, insulin was <21 pmol/l in 8-35% of the patients and in all controls; C-peptide was >0.2 nmol/l in all insulinomas but not in the nesidioblastosis or in the controls; proinsulin was >5 pmol/l in all patients but not in the controls.
  • Concomitant C-peptide levels above 0.2 nmol/l also make the diagnosis of all our insulinoma patients, not the diagnosis of nesidioblastosis, while insulin levels have much less diagnostic accuracy.

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  • [ErratumIn] Eur J Endocrinol. 2007 Nov;157(5):693
  • (PMID = 17609405.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Blood Glucose; 0 / C-Peptide; 0 / Insulin; 9035-68-1 / Proinsulin
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17. Körner M, Waser B, Reubi JC, Miller LJ: CCK(2) receptor splice variant with intron 4 retention in human gastrointestinal and lung tumours. J Cell Mol Med; 2010 Apr;14(4):933-43
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  • [Title] CCK(2) receptor splice variant with intron 4 retention in human gastrointestinal and lung tumours.
  • The wild-type cholecystokinin type 2 (CCK(2)) receptor is expressed in many gastrointestinal and lung tumours.
  • A splice variant of the CCK(2) receptor with retention of intron 4 (CCK(2)Ri4sv) showing constitutive activity associated with increased tumour growth was described in few colorectal, pancreatic and gastric cancers.
  • Given the potential functional and clinical importance of this spliceoform, its occurrence was quantitatively characterized in a broad collection of 81 gastrointestinal and lung tumours, including insulinomas, ileal carcinoids, gastrointestinal stromal tumours (GIST), gastric, colorectal and pancreatic ductal adenocarcinomas, cholangiocellular and hepatocellular carcinomas, small cell lung cancers (SCLC), non-SCLC (nSCLC) and bronchopulmonary carcinoids, as well as 21 samples of corresponding normal tissues.
  • Wild-type CCK(2) receptor transcripts were found in the vast majority of tumours and normal tissues.
  • CCK(2)Ri4sv mRNA expression was present predominantly in insulinomas (incidence 100%), GIST (100%) and SCLC (67%), but rarely in pancreatic, colorectal and gastric carcinomas and nSCLC.
  • It was not found in wild-type CCK(2) receptor negative tumours or any normal tissues tested.
  • CCK(2)Ri4sv transcript levels in individual tumours were low, ranging from 0.02% to 0.14% of total CCK(2) receptor transcripts.
  • In conclusion, the CCK(2)Ri4sv is a marker of specific gastrointestinal and lung tumours.

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  • (PMID = 19627395.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R37 DK032878-27; United States / NIDDK NIH HHS / DK / R01 DK032878; United States / NIDDK NIH HHS / DK / R37 DK032878; United States / NIDDK NIH HHS / DK / DK032878-27; United States / NIDDK NIH HHS / DK / DK32878
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, Cholecystokinin B
  • [Other-IDs] NLM/ NIHMS144707; NLM/ PMC2888751
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18. Oertli D: [Current concepts in minimal invasive endocrine surgery]. Ther Umsch; 2005 Feb;62(2):90-5
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  • Prerequisits for all of these approaches are a positive preoperative localisation of the adenoma, an intraoperative parathormone testing, and the respective surgical experience in the minimal invasive technique.
  • The experience with the laparoscopic approach to endocrine pancreatic tumours is still limited.
  • Good indications are insulinomas that are located anteriorly or within the tail of the pancreatic gland.
  • Nowadays, laparoscopic enucleation of such tumours and tail resections become feasable and safe.
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / surgery. Aged. Female. Humans. Insulinoma / surgery. Length of Stay. Male. Pancreatic Neoplasms / surgery. Parathyroid Neoplasms / diagnosis. Parathyroid Neoplasms / surgery. Patient Selection. Postoperative Complications. Safety. Time Factors

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  • (PMID = 15756917.001).
  • [ISSN] 0040-5930
  • [Journal-full-title] Therapeutische Umschau. Revue thérapeutique
  • [ISO-abbreviation] Ther Umsch
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 52
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19. Ramos E, Baron S, Sentanac S, Touati G, Picherot G: [Hypoglycemia associated with oral sulfonylurea hypoglycaemic agents in an 11-year-old girl]. Arch Pediatr; 2005 Jul;12(7):1109-11
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  • [Transliterated title] Hypoglycémie liée à la prise volontaire de sulfamides hypoglycémiants chez une enfant de 11 ans.
  • CASE REPORT: We report the case of an 11-year-old girl who presented recurrent hypoglycemia with endogenous hyperinsulinism (high insulin and C-peptide concentrations).
  • The morphological investigations didn't find insulinoma.
  • CONCLUSION: The sulfonylurea drugs can mimic an endogenous hyperinsulinism and mislead the diagnostic to an insulinoma suspicion and lead to a surgical exploration.
  • [MeSH-minor] Child. Diagnosis, Differential. Female. Humans. Hyperinsulinism / diagnosis. Insulinoma / diagnosis

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  • (PMID = 15925501.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Sulfonylurea Compounds
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20. Kang TW, Lee KT, Ryu MK, Moon W, Lee SS, Lee SY, Hwang JY, Lee JK, Heo JS, Choi SH, Kim SH, Paik SW, Rhee JC: [Clinical features of neuroendocrine tumor of the pancreas: single center study]. Korean J Gastroenterol; 2006 Aug;48(2):112-8
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  • [Title] [Clinical features of neuroendocrine tumor of the pancreas: single center study].
  • BACKGROUND/AIMS: Pancreatic neuroendocrine tumors (PNET) are rare and manifest as functioning tumor (FT) or non-functioning tumor (NFT).
  • Although malignant changes are observed in some cases, its prognosis is better than pancreatic cancer.
  • RESULTS: PNET included 6 insulinomas, 4 gastrinomas, 1 glucagonoma, 1 somatostatinoma and 31 NFT.
  • The major clinical manifestations were neuroglycopenic symptoms (100%) in insulinoma, abdominal ulcer symptoms (75%) in gastrinoma, dermatitis (100%) in glucagonoma, steatorrhea (100%) in somatostatinoma, and abdominal discomfort or pain (45%) in NFT.
  • In the recurrent NFT, the findings of diabetes mellitus (p=0.010), abnormal pancreatic duct (p=0.026), Whipple's operation (p=0.013) and tumor emboli (p=0.03) were more common than in non-recurrent NFT.
  • [MeSH-major] Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diabetes Mellitus / pathology. Female. Humans. Male. Middle Aged. Neoplastic Cells, Circulating / pathology. Pancreatic Ducts / abnormalities. Pancreatic Ducts / pathology. Whipple Disease / complications

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  • (PMID = 16929155.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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71. Hesselson D, Anderson RM, Beinat M, Stainier DY: Distinct populations of quiescent and proliferative pancreatic beta-cells identified by HOTcre mediated labeling. Proc Natl Acad Sci U S A; 2009 Sep 1;106(35):14896-901
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  • [Title] Distinct populations of quiescent and proliferative pancreatic beta-cells identified by HOTcre mediated labeling.
  • Pancreatic beta-cells are critical regulators of glucose homeostasis, and they vary dramatically in their glucose stimulated metabolic response and levels of insulin secretion.
  • It is unclear whether these parameters are influenced by the developmental origin of individual beta-cells.
  • Using HOTcre, a Cre-based genetic switch that uses heat-induction to precisely control the temporal expression of transgenes, we labeled two populations of beta-cells within the developing zebrafish pancreas.
  • These populations originate in distinct pancreatic buds and exhibit gene expression profiles suggesting distinct functions during development.
  • We find that the dorsal bud derived beta-cells are quiescent and exhibit a marked decrease in insulin expression postembryonically.
  • In contrast, ventral bud derived beta-cells proliferate actively, and maintain high levels of insulin expression compared with dorsal bud derived beta-cells.
  • Therapeutic strategies to regulate beta-cell proliferation and function are required to cure pathological states that result from excessive beta-cell proliferation (e.g., insulinoma) or insufficient beta-cell mass (e.g., diabetes mellitus).
  • Our data reveal the existence of distinct populations of beta-cells in vivo and should help develop better strategies to regulate beta-cell differentiation and proliferation.


72. de Herder WW, Kwekkeboom DJ, Valkema R, Feelders RA, van Aken MO, Lamberts SW, van der Lely AJ, Krenning EP: Neuroendocrine tumors and somatostatin: imaging techniques. J Endocrinol Invest; 2005;28(11 Suppl International):132-6
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  • [Title] Neuroendocrine tumors and somatostatin: imaging techniques.
  • Tumors and metastases bearing the somatostatin receptor subtypes 2 (SSTR2) or SSTR5 can be visualized in vivo after injection of radiolabeled octapeptide somatostatin analogs like 111In-pentetreotide.
  • The sensitivity of 111In-pentetreotide scintigraphy for the detection of carcinoid tumors is 86-95%.
  • The sensitivity of 111In-pentetreotide scintigraphy for the detection of gastrinomas, vasoactive intestinal polypeptide-secreting tumors, and glucagonomas as well as clinically non-functioning lesions is 75-100%.
  • However, for insulinoma this is 50-60%.
  • Most GH- and TSH-secreting pituitary adenomas can be visualized using 111In-pentetreotide.
  • 111In-pentetreotide scintigraphy has been successful for the localization of extra-pituitary ACTH-secreting tumors and their metastases, and especially for occult tumors.
  • [MeSH-major] Neuroendocrine Tumors / radionuclide imaging. Somatostatin
  • [MeSH-minor] Carcinoid Tumor / radionuclide imaging. Gastrointestinal Neoplasms / radionuclide imaging. Humans. Indium Radioisotopes. Paraganglioma / radionuclide imaging. Pheochromocytoma / radionuclide imaging. Pituitary Neoplasms / radionuclide imaging. Receptors, Somatostatin / analysis

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  • (PMID = 16625862.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide
  • [Number-of-references] 49
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73. Mabrut JY, Fernandez-Cruz L, Azagra JS, Bassi C, Delvaux G, Weerts J, Fabre JM, Boulez J, Baulieux J, Peix JL, Gigot JF, Hepatobiliary and Pancreatic Section (HBPS) of the Royal Belgian Society of Surgery, Belgian Group for Endoscopic Surgery (BGES), Club Coelio: Laparoscopic pancreatic resection: results of a multicenter European study of 127 patients. Surgery; 2005 Jun;137(6):597-605
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  • [Title] Laparoscopic pancreatic resection: results of a multicenter European study of 127 patients.
  • BACKGROUND: The reported experience with laparoscopic pancreatic resections (LPR) remains limited to case reports or small series of patients.
  • Detailed questionnaires were used, focusing on patients, tumors, operative data, and late outcome.
  • RESULTS: During the study period, 127 patients with presumed pancreatic neoplasms were enrolled in this series.
  • Final diagnoses included benign pancreatic diseases in 111 patients (87%; insulinoma: 22, neuroendocrine neoplasm: 20, mucinous cystadenoma: 26, serous cystadenoma: 21, chronic pancreatitis: 11, others: 11), and 16 patients (13%) had malignant pancreatic diseases (insulinoma: 3, neuroendocrine neoplasm: 5, ductal adenocarcinoma: 4, cystadenocarcinoma: 2, renal metastases: 2).
  • Five patients with presumed benign pancreatic disease had malignancy at final pathology.
  • The median tumor size was 30 mm (range, 5-120 mm); 89% of tumors were located in the left pancreas.
  • The rate of overall postoperative pancreatic-related complications was 31%, including a 17% rate of clinical pancreatic fistula.
  • During a median follow-up of 15 months (range, 3-47 months), 23% of the patients with pancreatic malignancies had tumor recurrence.
  • CONCLUSIONS: LPR is feasible and safe in selected patients with presumed benign and distal pancreatic tumors.
  • The management of the pancreatic stump remains a challenge.
  • The role of LPR for pancreatic malignancies remains controversial.
  • [MeSH-major] Laparoscopy. Pancreatectomy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Follow-Up Studies. Humans. Length of Stay. Neoplasm Recurrence, Local. Reoperation. Retrospective Studies. Treatment Outcome

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  • (PMID = 15962401.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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74. Happel B, Niederle B, Puespoek A, Ba-Ssalamah A, Schima W: [Benign neuroendocrine and other rare benign tumors of the pancreas]. Radiologe; 2008 Aug;48(8):752-63
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  • [Title] [Benign neuroendocrine and other rare benign tumors of the pancreas].
  • [Transliterated title] Benigne neuroendokrine und andere seltene benigne Tumoren des Pankreas.
  • Neuroendocrine tumors (NET) of the pancreas are rare neoplasms, which arise from cells of the islets of Langerhans.
  • The most common NET are the insulinoma, gastrinoma and hormone inactive NET.
  • [MeSH-major] Image Enhancement / methods. Magnetic Resonance Imaging / methods. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis. Tomography, X-Ray Computed / methods. Ultrasonography / methods

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  • (PMID = 18633589.001).
  • [ISSN] 0033-832X
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 41
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75. Goh BK, Ooi LL, Cheow PC, Tan YM, Ong HS, Chung YF, Chow PK, Wong WK, Soo KC: Accurate preoperative localization of insulinomas avoids the need for blind resection and reoperation: analysis of a single institution experience with 17 surgically treated tumors over 19 years. J Gastrointest Surg; 2009 Jun;13(6):1071-7
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  • [Title] Accurate preoperative localization of insulinomas avoids the need for blind resection and reoperation: analysis of a single institution experience with 17 surgically treated tumors over 19 years.
  • INTRODUCTION: Presently, the need for and choice of preoperative localization tests for insulinomas remain controversial.
  • MATERIALS AND METHODS: From 1990 to 2008, 17 patients with a clinical and biochemical diagnosis of an insulinoma who underwent surgery were retrospectively reviewed.
  • The diagnosis of all insulinomas were confirmed pathologically.
  • RESULTS: All tumors were localized preoperatively and an average of 2.2 preoperative localization studies including 1.4 noninvasive studies and 0.8 invasive studies were utilized per patient.
  • Invasive localization modalities were more sensitive (92%) than noninvasive modalities in localizing insulinomas (71%).
  • Fifteen of 17 tumors (88%) were localized intraoperatively via inspection/palpation and/or intraoperative ultrasonography.
  • Both insulinomas which were not localized intraoperatively were localized correctly to the distal pancreas via preoperative transhepatic portal venous sampling.
  • CONCLUSION: Accurate preoperative localization of insulinomas is useful as it eliminates the need for blind distal pancreatectomy and avoids reoperation.
  • Complete surgical resection is the treatment of choice, and whenever possible, a pancreas-sparing approach such as enucleation should be adopted.
  • [MeSH-major] Insulinoma / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 19291334.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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76. Alliouachene S, Tuttle RL, Boumard S, Lapointe T, Berissi S, Germain S, Jaubert F, Tosh D, Birnbaum MJ, Pende M: Constitutively active Akt1 expression in mouse pancreas requires S6 kinase 1 for insulinoma formation. J Clin Invest; 2008 Nov;118(11):3629-38
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  • [Title] Constitutively active Akt1 expression in mouse pancreas requires S6 kinase 1 for insulinoma formation.
  • Factors that promote pancreatic beta cell growth and function are potential therapeutic targets for diabetes mellitus.
  • In mice, genetic experiments suggest that signaling cascades initiated by insulin and IGFs positively regulate beta cell mass and insulin secretion.
  • Akt and S6 kinase (S6K) family members are activated as part of these signaling cascades, but how the interplay between these proteins controls beta cell growth and function has not been determined.
  • Here, we found that although transgenic mice overexpressing the constitutively active form of Akt1 under the rat insulin promoter (RIP-MyrAkt1 mice) had enlarged beta cells and high plasma insulin levels, leading to improved glucose tolerance, a substantial proportion of the mice developed insulinomas later in life, which caused decreased viability.
  • This oncogenic transformation tightly correlated with nuclear exclusion of the tumor suppressor PTEN.
  • The resulting mice displayed reduced insulinemia and glycemia compared with RIP-MyrAkt1 mice due to a combined effect of improved insulin secretion and insulin sensitivity.
  • Importantly, although the increase in beta cell size in RIP-MyrAkt1 mice was not affected by S6K1 deficiency, the hyperplastic transformation required S6K1.
  • Our results therefore identify S6K1 as a critical element for MyrAkt1-induced tumor formation and suggest that it may represent a useful target for anticancer therapy downstream of mTOR.
  • [MeSH-major] Insulinoma / metabolism. Pancreas / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Ribosomal Protein S6 Kinases / metabolism
  • [MeSH-minor] Animals. Cell Size. Crosses, Genetic. Disease Models, Animal. Insulin / blood. Insulin / genetics. Insulin / metabolism. Insulin-Secreting Cells / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. Promoter Regions, Genetic. Rats


77. Yang YM, Liu TH, Chen YJ, Jiang WJ, Qian JM, Lu X, Gao J, Wu SF, Sang XT, Chen J: Chromosome 1q loss of heterozygosity frequently occurs in sporadic insulinomas and is associated with tumor malignancy. Int J Cancer; 2005 Nov 1;117(2):234-40
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  • [Title] Chromosome 1q loss of heterozygosity frequently occurs in sporadic insulinomas and is associated with tumor malignancy.
  • The pathogenesis of sporadic insulinomas is not clear, and there are no reliable genetic determinants that are useful to distinguish malignant and benign forms of this tumor.
  • It was reported that 1q LOH might contribute to pathogenesis in gastrinomas and was correlated with tumor progression.
  • However, little data are available on 1q LOH in sporadic insulinomas.
  • In our study, we determine whether 1q LOH occurs in sporadic insulinomas and is associated with tumor malignancy by performing 1q allelotyping with 17 markers in 40 tumors and pair normal DNA.
  • Thirty-five (88%) insulinomas had 1q LOH.
  • Of the 35 insulinomas with 1q LOH, 14 (40%) had 1q21.3-23.2 LOH over a 7.5 cM region (SRO-1), whereas LOH in 21 tumors (60%) occurred at 1q31.3 over an 11.4 cM area (SRO-2).
  • Of 24 tumors without MEN1 LOH, 20 had either SRO-1 or SRO-2 LOH (83%), whereas in 16 tumors with MEN1 LOH, 9 were shown to have LOH at either SRO-1 or SRO-2 (56%) (p = 0.065).
  • This result suggests that LOH at 2 SRO might be MEN1 gene independent and may contribute to the pathogenesis in a subset of insulinomas without MEN1 gene LOH.
  • The presence of 1q21.3-23.2 LOH is significantly associated with malignancy of insulinomas (p = 0.014).
  • The high frequency of LOH at 1q 21.3-23.2 and 1q31.3 suggests these 2 areas may harbor putative tumor suppressor genes that may play an important role in the tumorigenesis of a subset of insulinomas.
  • LOH at 1q21.3-23.2, which was associated with tumor malignancy, could be one of the genetic markers for identifying malignancy in sporadic insulinomas.
  • [MeSH-major] Chromosomes, Human, Pair 1. Insulinoma / genetics. Loss of Heterozygosity. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosome Mapping. DNA, Neoplasm / genetics. Female. Humans. Insulin / blood. Male. Microsatellite Repeats. Middle Aged

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  • (PMID = 15900598.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Insulin
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78. van Erp M, Kooistra H, Galac S, Kirpensteijn J: [Insulinoma and diabetes mellitus in a dog. Call to refer dogs with insulinoma for examination and surgery]. Tijdschr Diergeneeskd; 2007 Jan 1;132(1):956-9
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  • [Title] [Insulinoma and diabetes mellitus in a dog. Call to refer dogs with insulinoma for examination and surgery].
  • [Transliterated title] Het Insulinoom en Diabetes Mellitus bij de hond. Oproep tot het doorsturen van honden met insulinoom voor onderzoek en operatie.
  • [MeSH-major] Diabetes Mellitus / veterinary. Dog Diseases / diagnosis. Dog Diseases / surgery. Insulinoma / veterinary. Referral and Consultation

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  • (PMID = 17334099.001).
  • [ISSN] 0040-7453
  • [Journal-full-title] Tijdschrift voor diergeneeskunde
  • [ISO-abbreviation] Tijdschr Diergeneeskd
  • [Language] dut
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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79. Gustaviani R, Soewondo P: Insulinoma. Acta Med Indones; 2007 Jan-Mar;39(1):49
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  • [Title] Insulinoma.
  • [MeSH-major] Insulinoma / diagnosis

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  • (PMID = 17297210.001).
  • [ISSN] 0125-9326
  • [Journal-full-title] Acta medica Indonesiana
  • [ISO-abbreviation] Acta Med Indones
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Indonesia
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80. Bose AK, Mocanu MM, Carr RD, Brand CL, Yellon DM: Glucagon-like peptide 1 can directly protect the heart against ischemia/reperfusion injury. Diabetes; 2005 Jan;54(1):146-51
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  • Glucagon-like peptide 1 (GLP-1), a gut incretin hormone that stimulates insulin secretion, also activates antiapoptotic signaling pathways such as phosphoinositide 3-kinase and mitogen-activated protein kinase in pancreatic and insulinoma cells.
  • This finding may represent a new therapeutic potential for this class of drug currently undergoing clinical trials in the treatment of type 2 diabetes.
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Butadienes / pharmacology. Chromones / pharmacology. Disease Models, Animal. Enzyme Inhibitors / pharmacology. Glucagon-Like Peptide 1. Heart Rate / drug effects. In Vitro Techniques. Insulin / secretion. MAP Kinase Signaling System / drug effects. MAP Kinase Signaling System / physiology. Male. Morpholines / pharmacology. Myocardial Infarction / pathology. Myocardial Infarction / prevention & control. Nitriles / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Rats. Rats, Sprague-Dawley. Time Factors

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  • (PMID = 15616022.001).
  • [ISSN] 0012-1797
  • [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 / Butadienes; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Insulin; 0 / Morpholines; 0 / Nitriles; 0 / Peptide Fragments; 0 / Protein Precursors; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 89750-14-1 / Glucagon-Like Peptide 1; 9007-92-5 / Glucagon; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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81. Schulte BM, Kramer M, Ansems M, Lanke KH, van Doremalen N, Piganelli JD, Bottino R, Trucco M, Galama JM, Adema GJ, van Kuppeveld FJ: Phagocytosis of enterovirus-infected pancreatic beta-cells triggers innate immune responses in human dendritic cells. Diabetes; 2010 May;59(5):1182-91
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  • [Title] Phagocytosis of enterovirus-infected pancreatic beta-cells triggers innate immune responses in human dendritic cells.
  • OBJECTIVE: Type 1 diabetes is a chronic endocrine disorder in which enteroviruses, such as coxsackie B viruses and echoviruses, are possible environmental factors that can trigger or accelerate disease.
  • The development or acceleration of type 1 diabetes depends on the balance between autoreactive effector T-cells and regulatory T-cells.
  • This balance is particularly influenced by dendritic cells (DCs).
  • The goal of this study was to investigate the interaction between enterovirus-infected human pancreatic islets and human DCs.
  • RESEARCH DESIGN AND METHODS: In vitro phagocytosis of human or porcine primary islets or Min6 mouse insuloma cells by DCs was investigated by flow cytometry and confocal analysis.
  • RESULTS: In this study, we show that both mock- and coxsackievirus B3 (CVB3)-infected human and porcine pancreatic islets were efficiently phagocytosed by human monocyte-derived DCs.
  • Studies with murine Min6 insuloma cells, which were also efficiently phagocytosed, revealed that increased ISG expression in DCs upon encountering CVB-infected cells resulted in an antiviral state that protected DCs from subsequent enterovirus infection.
  • The observed innate antiviral responses depended on RNA within the phagocytosed cells, required endosomal acidification, and were type I interferon dependent.
  • CONCLUSIONS: Human DCs can phagocytose enterovirus-infected pancreatic cells and subsequently induce innate antiviral responses, such as induction of RLHs.
  • [MeSH-major] Dendritic Cells / immunology. Enterovirus / physiology. Immunity, Innate / immunology. Insulin-Secreting Cells / cytology. Insulin-Secreting Cells / virology. Phagocytosis / immunology
  • [MeSH-minor] Animals. Cells, Cultured. Humans. Islets of Langerhans / cytology. Islets of Langerhans / immunology. Islets of Langerhans / virology. Mice. Swine. Tumor Cells, Cultured

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  • (PMID = 20071599.001).
  • [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
  • [Other-IDs] NLM/ PMC2857898
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82. Bazzi W, Renon M, Vercherat C, Hamze Z, Lacheretz-Bernigaud A, Wang H, Blanc M, Roche C, Calender A, Chayvialle JA, Scoazec JY, Cordier-Bussat M: MEN1 missense mutations impair sensitization to apoptosis induced by wild-type menin in endocrine pancreatic tumor cells. Gastroenterology; 2008 Nov;135(5):1698-1709.e2
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  • [Title] MEN1 missense mutations impair sensitization to apoptosis induced by wild-type menin in endocrine pancreatic tumor cells.
  • BACKGROUND & AIMS: Missense mutations account for 30% of mutations identified in patients with the multiple endocrine neoplasia type 1 (MEN1) syndrome.
  • METHODS: From the INS-1 insulinoma cell line, we established clones conditionally over expressing wild-type (WT) menin or its A160T, H317Y, and A541T variants.
  • RESULTS: WT menin over expression sensitized INS-r3 cells to apoptosis through amplification of caspase-3 activation, increased p53 acetylation, and accelerated p21 activation; moreover, over expressed WT menin could be recovered in p53-containing complexes.
  • CONCLUSIONS: Taking advantage of a new endocrine cellular model, we show a loss of function for 2 missense disease-related menin mutants and for a controversial variant as well.
  • [MeSH-major] Apoptosis / drug effects. DNA, Neoplasm / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Mutation, Missense. Pancreatic Neoplasms / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Cell Count. Cell Proliferation. Fluorescent Antibody Technique, Indirect. Gene Expression Regulation, Neoplastic. Genes, p53 / genetics. Humans. Immunoblotting. Polymerase Chain Reaction. Tumor Cells, Cultured


83. Schima W, Ba-Ssalamah A, Plank C, Kulinna-Cosentini C, Prokesch R, Tribl B, Sautner T, Niederle B: [Pancreas. Part II: Tumors]. Radiologe; 2006 May;46(5):421-37; quiz 438
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  • [Title] [Pancreas. Part II: Tumors].
  • Adenocarcinoma is the most common malignant pancreatic tumor, affecting the head in 60-70% of cases.
  • By the time of diagnosis, approximately 80% of tumors are unresectable.
  • Neuroendocrine tumors are mostly hypervascular.
  • Diagnosis of insulinoma is a challenge: they are <2 cm in 90% of cases and mostly hypervascular at CT or MRI.
  • A combination of contrast-enhanced MDCT, MRI, endosonography, and/or somatostatin receptor scintigraphy is used to detect these small tumors.
  • This review summarizes the imaging features of the most common pancreatic tumors and discusses the limitations of CT, MRI and endosonography.
  • [MeSH-major] Adenocarcinoma / diagnosis. Magnetic Resonance Imaging / methods. Pancreatic Neoplasms / diagnosis. Tomography, X-Ray Computed / methods. Ultrasonography / methods

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  • (PMID = 16715226.001).
  • [ISSN] 0033-832X
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 66
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84. Maj M, Gartner W, Ilhan A, Neziri D, Attems J, Wagner L: Expression of TAU in insulin-secreting cells and its interaction with the calcium-binding protein secretagogin. J Endocrinol; 2010 Apr;205(1):25-36
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  • [Title] Expression of TAU in insulin-secreting cells and its interaction with the calcium-binding protein secretagogin.
  • Tauopathies have been associated with Alzheimer's disease (AD), which frequently manifests together with diabetes mellitus type 2.
  • As pancreatic beta-cells and neurons share common electrophysiological properties, we investigated the appearance of TAU (listed as MAPT in the HUGO and MGI Databases) protein at the islets of Langerhans and beta-cell-derived cell lines which highly express the neuroendocrine-specific protein SCGN.
  • Co-localization of TAU and SCGN within insulinoma cells and islets of Langerhans mainly restricted to insulin-positive beta-cells was demonstrated by confocal microscopy.
  • Motivated by these findings, we looked if SCGN overexpression could exert protective function on Rin-5F cells, which showed differences in TAU levels.
  • Our findings demonstrated for the first time the association of TAU and the calcium-binding protein SCGN and support earlier results implicating that beta-cells might represent an extra cerebral site of tauopathy.
  • [MeSH-major] Calcium-Binding Proteins / metabolism. Insulin-Secreting Cells / metabolism. tau Proteins / metabolism
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Line, Tumor. Disease Models, Animal. Insulinoma / metabolism. Insulinoma / pathology. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Protein Isoforms / metabolism. Rats. Secretagogins

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  • (PMID = 20061514.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0400074; United Kingdom / Medical Research Council / / G0502157; United Kingdom / Medical Research Council / / G0900652
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Protein Isoforms; 0 / Secretagogins; 0 / tau Proteins; SY7Q814VUP / Calcium
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85. Ravassard P, Emilie Bricout-Neveu, Hazhouz Y, Pechberty S, Mallet J, Czernichow P, Scharfmann R: A new strategy to generate functional insulin-producing cell lines by somatic gene transfer into pancreatic progenitors. PLoS One; 2009;4(3):e4731
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  • [Title] A new strategy to generate functional insulin-producing cell lines by somatic gene transfer into pancreatic progenitors.
  • BACKGROUND: There is increasing interest in developing human cell lines to be used to better understand cell biology, but also for drug screening, toxicology analysis and future cell therapy.
  • In the endocrine pancreatic field, functional human beta cell lines are extremely scarce.
  • On the other hand, rodent insulin producing beta cells have been generated during the past years with great success.
  • Many of such cell lines were produced by using transgenic mice expressing SV40T antigen under the control of the insulin promoter, an approach clearly inadequate in human.
  • Our objective was to develop and validate in rodent an alternative transgenic-like approach, applicable to human tissue, by performing somatic gene transfer into pancreatic progenitors that will develop into beta cells.
  • METHODS AND FINDINGS: In this study, rat embryonic pancreases were transduced with recombinant lentiviral vector expressing the SV40T antigen under the control of the insulin promoter.
  • Transduced tissues were next transplanted under the kidney capsule of immuno-incompetent mice allowing insulinoma development from which beta cell lines were established.
  • Gene expression profile, insulin content and glucose dependent secretion, normalization of glycemia upon transplantation into diabetic mice validated the approach to generate beta cell lines.
  • CONCLUSIONS: Somatic gene transfer into pancreatic progenitors represents an alternative strategy to generate functional beta cell lines in rodent.
  • Moreover, this approach can be generalized to derive cells lines from various tissues and most importantly from tissues of human origin.
  • [MeSH-major] Insulin-Secreting Cells / cytology. Insulin-Secreting Cells / transplantation. Pancreas / cytology. Stem Cells / cytology. Transduction, Genetic
  • [MeSH-minor] Animals. Cell Line. Genetic Vectors. Insulin / genetics. Insulinoma. Lentivirus / genetics. Mice. Mice, Transgenic. Promoter Regions, Genetic. Rats. Stem Cell Transplantation


86. Farkas G, Leindler L, Farkas G Jr: Safe closure technique for distal pancreatic resection. Langenbecks Arch Surg; 2005 Feb;390(1):29-31
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  • [Title] Safe closure technique for distal pancreatic resection.
  • BACKGROUND AND AIMS: Various methods had previously been employed to manage the proximal pancreas after distal resection (mattress sutures with duct ligation; pancreato-enterostomy or stapling with stainless steel staples, etc.
  • PATIENTS/METHODS: In the past 10 years, distal pancreatic resection in 90 patients [62 men, 28 women, mean age 52 (24-72)] years) was followed by closure of the resection surfaces with absorbable lactomer clips.
  • Indications for distal resection (with or without splenectomy) were: focal pancreatic necrosis, spontaneous pancreatic fistulas, abscess, pseudocyst, traumatic disruption, segmental chronic obstructive pancreatitis in the tail, and benign (cystadenoma, or insulinoma) or malignant tumours.
  • RESULTS: The postoperative period was uneventful in all these patients, without any complications (pancreatic fistula, abscess or bleeding).
  • CONCLUSIONS: The clinical results clearly demonstrated that the application of absorbable lactomer staples for closure of the transected margin of the pancreas is a safe alternative to the standard closure technique.
  • These staples can be applied in all cases when distal pancreatic resection is indicated for benign or malignant disorders or a traumatically injured pancreatic gland.
  • [MeSH-major] Pancreas / surgery. Polymers. Suture Techniques. Sutures
  • [MeSH-minor] Absorbable Implants. Female. Humans. Male. Middle Aged. Pancreatic Diseases / surgery. Postoperative Complications / epidemiology. Surgical Instruments

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  • (PMID = 15338310.001).
  • [ISSN] 1435-2443
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Polymers; 12770-88-6 / polysorb
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87. Grozinsky-Glasberg S, Franchi G, Teng M, Leontiou CA, Ribeiro de Oliveira A Jr, Dalino P, Salahuddin N, Korbonits M, Grossman AB: Octreotide and the mTOR inhibitor RAD001 (everolimus) block proliferation and interact with the Akt-mTOR-p70S6K pathway in a neuro-endocrine tumour cell Line. Neuroendocrinology; 2008;87(3):168-81
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  • [Title] Octreotide and the mTOR inhibitor RAD001 (everolimus) block proliferation and interact with the Akt-mTOR-p70S6K pathway in a neuro-endocrine tumour cell Line.
  • BACKGROUND/AIM: The mode of action of the somatostatin analog octreotide on neuro-endocrine tumour proliferation is largely unknown.
  • Overexpression of the proto-oncogene Akt/PKB (protein kinase B) has been demonstrated in certain neuro-endocrine tumours: Akt activates downstream proteins including mTOR and p70S6K, which play an important role in cell proliferation.
  • RAD001 (everolimus) is a novel agent that is being trialled in the treatment of neuro-endocrine tumours, and is known to interact with mTOR.
  • We explored the mechanism of action of octreotide, RAD001, and their combination on cell proliferation and kinase activation in a neuro-endocrine tumour cell line (rat insulinoma cell line, INS1).
  • METHODS: Proliferation assays were used to determine the effects of octreotide, RAD001, and their combination on cell proliferation.
  • CONCLUSIONS: In this cell model, octreotide and RAD001 appear to act through a similar pathway and inhibit the Akt-mTOR-p70S6 kinase pathway downstream of Akt.
  • [MeSH-major] Neuroendocrine Tumors / metabolism. Octreotide / pharmacology. Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Sirolimus / analogs & derivatives
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Everolimus. Rats. Signal Transduction / drug effects. Signal Transduction / physiology. TOR Serine-Threonine Kinases. Tumor Cells, Cultured

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  • [Copyright] (c) 2007 S. Karger AG, Basel
  • (PMID = 18025810.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; RWM8CCW8GP / Octreotide; W36ZG6FT64 / Sirolimus
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88. Cui W, De Jesus K, Zhao H, Takasawa S, Shi B, Srikant CB, Liu JL: Overexpression of Reg3alpha increases cell growth and the levels of cyclin D1 and CDK4 in insulinoma cells. Growth Factors; 2009 Jun;27(3):195-202
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  • [Title] Overexpression of Reg3alpha increases cell growth and the levels of cyclin D1 and CDK4 in insulinoma cells.
  • Regenerating gene (Reg) family protein Reg3alpha is normally expressed in pancreatic acinar and endocrine cells.
  • In order to explore its effect on islet beta-cell replication, insulinoma MIN6 cells were stably transfected with murine Reg3alpha cDNA.
  • In MTT cell proliferation assay, Reg3alpha-overexpressing cells exhibited a 2-fold increase in the rate of cell growth.
  • In order to investigate the intracellular mechanism, we studied cell cycle regulatory proteins.
  • In Reg3alpha-expressing cells, we detected 2.2- and 2.5-fold increased levels of cyclin D1 and CDK4, respectively, which paralleled a 1.8-fold increase in the rate of Akt phosphorylation.
  • It is established that beta-cell replication is associated with increased cyclin D1 and CDK4 levels; deficiency in CDK4 or cyclin D2 results in reduced beta-cell mass and diabetes.
  • Our results suggest that Reg3alpha stimulates beta-cell replication, by activating Akt kinase and increasing the levels of cyclin D1/CDK4.
  • [MeSH-major] Cyclin D1 / metabolism. Cyclin-Dependent Kinase 4 / metabolism. Insulin-Secreting Cells / physiology. Insulinoma / metabolism. Proteins / physiology
  • [MeSH-minor] Animals. Antigens, Neoplasm. Biomarkers, Tumor. Cell Line, Tumor. Cell Proliferation. Lectins, C-Type. Mice. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 19343564.001).
  • [ISSN] 1029-2292
  • [Journal-full-title] Growth factors (Chur, Switzerland)
  • [ISO-abbreviation] Growth Factors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Proteins; 0 / pancreatitis-associated protein; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Akt1 protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / Cdk4 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
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89. Tongson-Ignacio JE, Honda SA, Bhagavan NV: Insulinoma, a rare neuroendocrine tumor: a case report. Hawaii Med J; 2005 Jan;64(1):9-11
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  • [Title] Insulinoma, a rare neuroendocrine tumor: a case report.
  • We report a case of Insulinoma, a rare neuroendocrine tumor with an incidence of approximately four per 5 million.
  • This case demonstrates the characteristic clinical, biochemical and histological features of an insulinoma, a rare benign neuroendocrine tumor where early recognition is important to ensure proper surgical treatment and prevent serious adverse consequences.
  • [MeSH-major] Insulinoma. Pancreatic Neoplasms
  • [MeSH-minor] Female. Humans. Immunoenzyme Techniques. Middle Aged. Pancreas / pathology. Treatment Outcome


90. Libé R, Chanson P: [Endocrine tumors of the pancreas (EPTs) in multiple endocrine neoplasia (MEN1): up-date on prognostic factors, diagnostic procedures and treatment]. Ann Endocrinol (Paris); 2007 Jun;68 Suppl 1:1-8
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  • [Title] [Endocrine tumors of the pancreas (EPTs) in multiple endocrine neoplasia (MEN1): up-date on prognostic factors, diagnostic procedures and treatment].
  • [Transliterated title] Les tumeurs endocrines du pancréas lors de la néoplasie endocrinienne multiple type 1 (NEM1): actualités sur les facteurs pronostiques, l'imagerie et le traitement.
  • Endocrine pancreatic tumors (EPTs) are uncommon tumors, representing 1-2% of all pancreatic neoplasms.
  • They are categorized on the basis of their clinical features into functioning and non-functioning tumors.
  • EPTs may be part of the multiple endocrine neoplasia type 1 (MEN 1), an autosomal dominant syndrome due to inactivating germline mutation of the menin gene.
  • Somatic mutations of menin are present in about 20% of sporadic neoplasms, particularly gastrinomas and insulinomas.
  • The most prevalent are the gastrinomas (20-60%), then the insulinomas (5-10%), the glucagonamas and VIPomas (6-10%), whereas the nonfunctioning EPTs are present in 20-40% of patients.
  • Among the different imaging techniques, echoendoscopy, computed tomography (CT) and magnetic resonance imaging (MRI) are indicated for the detection of the primary tumor, but (III)In-octreotide scintigraphy has the highest sensitivity for detecting metastases.
  • The choice of treatment is still debated and is different when the tumor occurs as a part of the MEN syndrome.
  • The surgical treatment is the first choice for insulinomas and is more controversial for gastrinomas.
  • Chemotherapy, which is generally proposed as a combination of streptozotocin (STZ) and 5-fluorouracil (5-FU) or doxorubicin, is indicated when the tumors tend to grow.
  • Interferon-alpha (IFN-alpha) stimulates the immune system, blocks the tumor cells in the G1/S-phase of the cell cycle, inhibits protein and hormone synthesis and inhibits angionenesis.
  • Treatment with IFN has been shown to produce symptomatic response in 40-60% of patients, a biochemical response in 30-60% and tumor shrinkage in 10-15%.
  • [MeSH-major] Carcinoma, Islet Cell. Multiple Endocrine Neoplasia Type 1


91. Stamatakos M, Safioleas C, Tsaknaki S, Safioleas P, Iannescu R, Safioleas M: Insulinoma: a rare neuroendocrine pancreatic tumor. Chirurgia (Bucur); 2009 Nov-Dec;104(6):669-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insulinoma: a rare neuroendocrine pancreatic tumor.
  • Insulinomas are functional endocrine tumors originating from the pancreatic b-cells.
  • In 1902 Nicholls described the first adenoma of pancreatic islets, while the first insulinoma was described in 1927 in Mayo Clinic, which was dissected two years later in 1929 in Toronto.
  • The first enucleation of insulinoma took place in a St. Jouis hospital in 1931, and after four years, in 1935, Whipple described the classic diagnostic triad: symptoms of fasting hypoglycemia or fatigue, blood glucose levels under 50 mg/dl and disappearance of symptoms after glucose administration.
  • [MeSH-major] Insulinoma / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis. Rare Diseases


92. Pedersen KB, Buckley RS, Scioneaux R: Glucose induces expression of rat pyruvate carboxylase through a carbohydrate response element in the distal gene promoter. Biochem J; 2010 Mar 1;426(2):159-70
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  • Pyruvate carboxylase is an enzyme of the so-called pyruvate cycling pathways, which have been proposed to contribute to glucose-stimulated insulin secretion in pancreatic beta-cells.
  • In the rat insulinoma cell line 832/13, transcripts from both the distal and proximal gene promoter for pyruvate carboxylase are up-regulated by glucose, with pyruvate carboxylase being expressed mainly from the distal gene promoter.
  • At position -408 to -392 relative to the transcription start site, the distal gene promoter was found to contain a ChoRE (carbohydrate response element).
  • [MeSH-minor] Animals. Base Sequence. Binding Sites. Cell Line, Tumor. Molecular Sequence Data. Protein Binding. Sequence Deletion. Transcriptional Activation

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  • (PMID = 20001964.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.4.1.1 / Pyruvate Carboxylase; IY9XDZ35W2 / Glucose
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93. Zitzer H, Wente W, Brenner MB, Sewing S, Buschard K, Gromada J, Efanov AM: Sterol regulatory element-binding protein 1 mediates liver X receptor-beta-induced increases in insulin secretion and insulin messenger ribonucleic acid levels. Endocrinology; 2006 Aug;147(8):3898-905
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sterol regulatory element-binding protein 1 mediates liver X receptor-beta-induced increases in insulin secretion and insulin messenger ribonucleic acid levels.
  • Pancreatic beta-cells and INS-1E insulinoma cells express only the LXRbeta isoform.
  • Activation of LXRbeta with the synthetic agonist T0901317 increased glucose-induced insulin secretion and insulin content, whereas deletion of the receptor in LXRbeta knockout mice severely blunted insulin secretion.
  • Analysis of gene expression in LXR agonist-treated INS-1E cells and islets from LXRbeta-deficient mice revealed that LXRbeta positively regulated expression of ATP-binding cassette transporter A1 (ABCA1), sterol regulatory element-binding protein 1 (SREBP-1), insulin, PDX-1, glucokinase, and glucose transporter 2 (Glut2).
  • Down-regulation of SREBP-1 expression with the specific small interfering RNA blocked basal and LXRbeta-induced expression of pancreatic duodenal homeobox 1 (PDX-1), insulin, and Glut2 genes.
  • SREBP-1 small interfering RNA also prevented an increase in insulin secretion and insulin content induced by T0901317.
  • Moreover, 5-(tetradecyloxy)-2-furoic acid, an inhibitor of the SREBP-1 target gene acetyl-coenzyme A carboxylase, blocked T0901317-induced stimulation of insulin secretion.
  • In conclusion, activation of LXRbeta in pancreatic beta-cells increases insulin secretion and insulin mRNA expression via SREBP-1-regulated pathway.
  • These data support the role of LXRbeta, SREBP-1, and cataplerosis/anaplerosis pathways in the control of insulin secretion in pancreatic beta-cells.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Insulin / genetics. Insulin / metabolism. Receptors, Cytoplasmic and Nuclear / metabolism. Sterol Regulatory Element Binding Protein 1 / metabolism
  • [MeSH-minor] Alternative Splicing. Animals. Cell Line, Tumor. Gene Expression Regulation / physiology. Glucose Intolerance / metabolism. Glucose Intolerance / physiopathology. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Hydrocarbons, Fluorinated. Insulinoma. Islets of Langerhans / cytology. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Orphan Nuclear Receptors. Pancreatic Neoplasms. RNA, Messenger / metabolism. RNA, Small Interfering. Sulfonamides / pharmacology. Trans-Activators / genetics. Trans-Activators / metabolism

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  • (PMID = 16644917.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Hydrocarbons, Fluorinated; 0 / Insulin; 0 / Orphan Nuclear Receptors; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Srebf1 protein, mouse; 0 / Sterol Regulatory Element Binding Protein 1; 0 / Sulfonamides; 0 / TO-901317; 0 / Trans-Activators; 0 / liver X receptor; 0 / pancreatic and duodenal homeobox 1 protein
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94. Yuan CL, Xu JF, Tong J, Yang H, He FR, Gong Q, Xiong P, Duan L, Fang M, Tan Z, Xu Y, Chen YF, Zheng F, Gong FL: B7-H4 transfection prolongs beta-cell graft survival. Transpl Immunol; 2009 Jul;21(3):143-9
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  • [Title] B7-H4 transfection prolongs beta-cell graft survival.
  • B7-H4, a recently discovered member of B7 family, can negatively regulate T cell responses.
  • However, it is not clear whether B7-H4 negatively function in cell transplantation.
  • In this study we investigated the immunosuppressive effect of B7-H4 on beta-cell transplantation.
  • An insulinoma cell line, NIT-1, transfected with B7-H4 (B7-H4-NIT) was established, and transplanted to diabetic C57BL/6 mice by intraperitoneal injection.
  • Proliferation assay of splenocytes in vitro showed that B7-H4-NIT suppressed alloreactive T cell activation.
  • The proportion of IFN-gamma-producing cells in recipient spleen was significantly reduced and the number of Treg cells was upregulated in B7-H4-NIT group compared to the control, EGFP-NIT.
  • More importantly, the survival time for recipients transplanted with B7-H4-NIT cells was significantly longer than that with EGFP-NIT cells.
  • These results indicate that B7-H4 transfection prolongs beta-cell graft survival.
  • [MeSH-major] Antigens, CD80 / immunology. Diabetes Mellitus, Experimental / surgery. Diabetes Mellitus, Type 1 / surgery. Graft Survival / immunology. Immunosuppression / methods. Insulin-Secreting Cells / transplantation
  • [MeSH-minor] Animals. Cell Line, Tumor. Green Fluorescent Proteins / immunology. Green Fluorescent Proteins / metabolism. Interferon-gamma / immunology. Interleukin-4 / immunology. Interleukin-4 / metabolism. Male. Mice. Mice, Inbred C57BL. T-Lymphocytes, Regulatory / immunology. Transfection. V-Set Domain-Containing T-Cell Activation Inhibitor 1

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  • (PMID = 19361556.001).
  • [ISSN] 1878-5492
  • [Journal-full-title] Transplant immunology
  • [ISO-abbreviation] Transpl. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / V-Set Domain-Containing T-Cell Activation Inhibitor 1; 0 / Vtcn1 protein, mouse; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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95. Oliveira CH, Berger K, Souza SC, Marui S, Khawali C, Hauache OM, Vieira JG, Maciel RM, Reis AF: [Continuous glucose monitoring: a critical appraisal after one year experience]. Arq Bras Endocrinol Metabol; 2005 Dec;49(6):983-90
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  • [Transliterated title] Monitorização contínua de glicose: análise crítica baseada em experiência ao longo de um ano.
  • Overall, 88% (n= 124) patients were diabetics (DM), 99 of them were insulin users.
  • Two tests came out very suggestive of "dumping", and in one case the CGMS supported the hypothesis of insulinoma.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Dumping Syndrome / diagnosis. Female. Humans. Hyperglycemia / prevention & control. Hypoglycemia / prevention & control. Infant. Linear Models. Male. Middle Aged. Statistics, Nonparametric. Time Factors

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  • (PMID = 16544024.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] Brazil
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96. Pasquali C, Sperti C, Baratella P, Liessi G, Pedrazzoli S: [Enucleation-resection of pancreatic neuroendocrine tumors: 25 years of experience]. Suppl Tumori; 2005 May-Jun;4(3):S59-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Enucleation-resection of pancreatic neuroendocrine tumors: 25 years of experience].
  • From 1980 to 2004, out of 109 patients who underwent surgery for neuroendocrine pancreatic tumor, 33 had a simple tumor excision.
  • Seventy-two percent of cases were insulinomas.
  • Age, sex, site and size of the tumor, associated diseases, hospital stay and complications were retrospectively reviewed by the clinical records.
  • Mean size of the tumor was 1.7 cm and 54.5% were in the pancreatic head; 78.8% of cases had medical associated diseases.
  • Complications were divided in early (related to pancreatic surgery, related to general open surgery and medical) and late events.
  • Complication related to pancreatic surgery were 6/33 (18%); 5 pancreatic fistulas (4 low output) and 1 acute pancreatitis, while 5/33 had a general surgery complication (2 leacking due to gastric and duodenal associated operations).
  • No patient was re-operated for pancreatic complications; 1 was reoperated for evisceration and 1 for hyper-parathyroidism in the early post-operative period.
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16437904.001).
  • [ISSN] 2283-5423
  • [Journal-full-title] I supplementi di Tumori : official journal of Società italiana di cancerologia ... [et al.]
  • [ISO-abbreviation] Suppl Tumori
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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97. Tessonnier L, Sebag F, Ghander C, De Micco C, Reynaud R, Palazzo FF, Conte-Devolx B, Henry JF, Mundler O, Taïeb D: Limited value of 18F-F-DOPA PET to localize pancreatic insulin-secreting tumors in adults with hyperinsulinemic hypoglycemia. J Clin Endocrinol Metab; 2010 Jan;95(1):303-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Limited value of 18F-F-DOPA PET to localize pancreatic insulin-secreting tumors in adults with hyperinsulinemic hypoglycemia.
  • CONTEXT: Fluorine-18-L-dihydroxyphenylalanine positron emission tomography (18F-FDOPA PET) imaging is increasingly used in the workup of neuroendocrine tumors.
  • It has been shown to be an accurate tool in the diagnosis of congenital hyperinsulinism, but limited information is available on its value in adult disease.
  • OBJECTIVE, PATIENTS, AND DESIGN: The objective of this study was to review our experience with 18F-FDOPA PET imaging in six consecutive patients with hyperinsulinemic hypoglycemia (HH) (four solitary insulinomas, one diffuse beta-cell hyperplasia, one malignant insulinoma).
  • 18F-FDOPA uptake was also evaluated in 37 patients (43 procedures) without HH or other pancreatic neuroendocrine tumors, which acted as a control group.
  • RESULTS: Using visual analysis, 18F-FDOPA-PET proved positive in only one case (a multiple endocrine neoplasia type 1 related insulinoma).
  • In diffuse beta-cell hyperplasia, the pancreatic uptake was similar to controls.
  • In the patient with liver metastases, the extent of disease was underestimated.
  • The pancreatic uptake was not statistically different between controls and hyperinsulinemic patients.
  • The main limitation for identifying insulinomas or beta-cell hyperplasia in adults appears to be to the 18F-FDOPA uptake and retention in the whole pancreas.
  • This drawback is potentially circumvented in focal hyperplasia in newborns due to a lower aromatic amino acid decarboxylase expression in the extralesional pancreatic parenchyma.
  • CONCLUSIONS: 18F-FDOPA PET is of limited value in localizing pancreatic insulin secreting tumors in adult HH.
  • [MeSH-major] Dihydroxyphenylalanine. Hyperinsulinism / complications. Hypoglycemia / complications. Insulinoma / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Insulin-Secreting Cells / pathology. Insulin-Secreting Cells / radionuclide imaging. Male. Middle Aged. Predictive Value of Tests. Retrospective Studies. Young Adult

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  • (PMID = 19915018.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 2C598205QX / fluorodopa F 18; 63-84-3 / Dihydroxyphenylalanine
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98. Kim SJ, Jeong DG, Jeong SK, Yoon TS, Ryu SE: Crystal structure of the major diabetes autoantigen insulinoma-associated protein 2 reveals distinctive immune epitopes. Diabetes; 2007 Jan;56(1):41-8
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  • [Title] Crystal structure of the major diabetes autoantigen insulinoma-associated protein 2 reveals distinctive immune epitopes.
  • Insulinoma-associated protein-2 (IA-2) is a major autoantigen in type 1 diabetes that occurs through autoimmune-mediated beta-cell destruction.
  • The structure reveals a canonical PTP domain with the closed WPD loop over the active site pocket, explaining the lack of enzyme activity in the native protein.
  • The structural interpretation of previous mutagenesis studies indicates that the B-cell epitopes are concentrated on two distinctive regions on peripheral loops of the central beta-sheet surrounding T-cell epitopes within the sheet.

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  • (PMID = 17192463.001).
  • [ISSN] 0012-1797
  • [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 / Autoantigens; 0 / BIRC3 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Membrane Proteins; EC 3.1.3.48 / PTPRN protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 1; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 8; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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99. Simpson M, Mojibian M, Barriga K, Scott FW, Fasano A, Rewers M, Norris JM: An exploration of Glo-3A antibody levels in children at increased risk for type 1 diabetes mellitus. Pediatr Diabetes; 2009 Dec;10(8):563-72
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  • AIMS: To determine whether Glo-3A, (formerly referred to as homologue of Glb1 or Glb1) antibodies are associated with islet autoimmunity (IA) in children at increased risk for type 1 diabetes (T1D) and to investigate their relation with environmental correlates of T1D.
  • Cases were positive for insulin, glutamic acid decarboxylase (GAD), or insulinoma-associated antigen-2 (IA-2) autoantibodies on two consecutive visits and either diagnosed with diabetes mellitus or still autoantibody positive when selected.
  • Adjusting for age, family history of T1D, and HLA-DR4 positivity, Glo-3A antibody levels were inversely associated with breast-feeding duration (beta = -0.08, p = 0.001) and directly associated with current intake of foods containing gluten (beta = 0.24, p = 0.007) in IA cases but not in controls.
  • Zonulin, a biomarker of gut permeability, was directly associated with Glo-3A antibody levels in cases (beta = 0.73, p = 0.003) but not in controls.

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  • (PMID = 19622083.001).
  • [ISSN] 1399-5448
  • [Journal-full-title] Pediatric diabetes
  • [ISO-abbreviation] Pediatr Diabetes
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK032493-16; United States / NIDDK NIH HHS / DK / R01 DK049654-03; United States / NIDDK NIH HHS / DK / DK049654-03; United States / NIDDK NIH HHS / DK / R01 DK032493-16; United States / NIDDK NIH HHS / DK / R01 DK050979; United States / NIDDK NIH HHS / DK / R01 DK049654; United States / NIDDK NIH HHS / DK / R01 DK032493
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / ICA512 autoantibody; 0 / Immunoglobulin G; 0 / zonulin; 9007-90-3 / Gliadin; 9012-63-9 / Cholera Toxin; EC 4.1.1.15 / Glutamate Decarboxylase
  • [Other-IDs] NLM/ NIHMS171434; NLM/ PMC2814050
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100. Han JH, Kim MH, Moon SH, Park SJ, Park DH, Lee SS, Seo DW, Lee SK, Kim SC, Han DJ: [Clinical characteristics and malignant predictive factors of pancreatic neuroendocrine tumors]. Korean J Gastroenterol; 2009 Feb;53(2):98-105
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  • [Title] [Clinical characteristics and malignant predictive factors of pancreatic neuroendocrine tumors].
  • BACKGROUND/AIMS: Neuroendocrine tumors (NET) of the pancreas are rare.
  • Its prognosis is better than pancreas adenocarcinoma due to the slow growth, however, malignant NET of the pancreas are observed.
  • The purposes of this study were to evaluate the clinical characteristics and to find the predictive factors of NET which are associated with malignancy and survival.
  • METHODS: We retrospectively evaluated the clinical outcomes of 122 patients with NET of the pancreas who were pathologically diagnosed at Asan Medical Center between 1990 and 2006.
  • The major clinical manifestations were abdominal pain (44.0%) in non-functional tumor, neuroglycopenic symptoms (100%) in insulinoma and diarrhea (60%) in gastrinoma.
  • Tumor size ranged from 4 to 140 mm (average 29.8+/-23.22).
  • Ninety cases (73.8%) were classified as benign tumors and 32 cases (26.2%) as malignant.
  • In multivariate analysis of clinical characteristics, large sized tumor (>20 mm, p=0.001) was confirmed as sole independent factor to predict malignant NET.
  • All patients with benign NET are still alive without recurrence.
  • Six out of 32 patients with malignant NET died at an average 40.3 months after diagnosis.
  • The factors indicating favorable outcome were small size of tumors (p=0.046), resection of primary tumor (p=0.000), absence of lymph node invasion (p=0.0116) and distant metastasis (p=0.0005).
  • CONCLUSIONS: Large NET of the pancreas, regardless of their functioning status, were more likely to be associated with malignancy and predictor of worse survival.
  • [MeSH-major] Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19237835.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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