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1. Hammerman MR: Organogenesis of the endocrine pancreas. Kidney Int; 2005 Nov;68(5):1953-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Organogenesis of the endocrine pancreas.
  • Organogenesis of the endocrine pancreas.
  • Embryonic pancreatic primordia transplanted into diabetic animal hosts undergo selective endocrine differentiation in situ and normalize glucose tolerance.
  • [MeSH-major] Diabetes Mellitus, Type 1 / surgery. Fetal Tissue Transplantation. Islets of Langerhans / embryology. Pancreas Transplantation. Transplantation, Heterologous

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  • (PMID = 16221174.001).
  • [ISSN] 0085-2538
  • [Journal-full-title] Kidney international
  • [ISO-abbreviation] Kidney Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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2. Nishida K, Shimoda S, Ichinose K, Araki E, Shichiri M: What is artificial endocrine pancreas? Mechanism and history. World J Gastroenterol; 2009 Sep 7;15(33):4105-10

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  • [Title] What is artificial endocrine pancreas? Mechanism and history.
  • The artificial endocrine pancreas is a feedback control instrument that regulates insulin delivery on a minute-by-minute basis according to measured blood glucose levels.
  • Only one type of bedside-type artificial endocrine pancreas is now available in Japan: STG-22 (Nikkiso Co. Ltd., Japan).
  • The bedside-type artificial endocrine pancreas has been proven to be useful not only as a therapeutic tool for diabetes mellitus, but also as an elegant research tool for investigating the pathophysiology of the disease, by using the euglycemic hyperinsulinemic glucose clamp technique.

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  • (PMID = 19725141.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Blood Glucose
  • [Number-of-references] 33
  • [Other-IDs] NLM/ PMC2738803
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3. Bock T, Pakkenberg B, Buschard K: Genetic background determines the size and structure of the endocrine pancreas. Diabetes; 2005 Jan;54(1):133-7

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  • [Title] Genetic background determines the size and structure of the endocrine pancreas.
  • Key parameters of the endocrine pancreas, such as islet number, islet mass, beta-cell mass, and alpha-cell mass, were studied in different strains of inbred mice to investigate the impact of genetic background on the size and structure of the endocrine pancreas.
  • ANCOVA showed that only mouse strain was statistically significant as an explanatory parameter for the number of islets.
  • Mouse strain, body weight, and pancreas mass reached statistical significance as explanatory parameters for the islet mass, with mouse strain as the most significant predictor.
  • These data show that genetic background is the most important predictor of both the number of islets and total islet volume.
  • We also conclude that inbred mice could be a valuable resource to identify the genes responsible for the size and structure of the endocrine pancreas.
  • [MeSH-major] Islets of Langerhans / anatomy & histology. Mice, Inbred Strains / genetics. Pancreas / anatomy & histology

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  • (PMID = 15616020.001).
  • [ISSN] 0012-1797
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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4. Igaz P, Igaz I, Rácz K, Tulassay Z: [Hereditary tumours of the endocrine pancreas]. Orv Hetil; 2006 Feb 5;147(5):195-200
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  • [Title] [Hereditary tumours of the endocrine pancreas].
  • [Transliterated title] Az endokrin pancreas öröklódó daganatai.
  • The pathogenesis, diagnosis and therapy of tumours originating from the endocrine pancreas represent one of the most exciting challenges of contemporary medicine.
  • Some of these tumours appear as part of four hereditary syndromes (multiple endocrine neoplasia type 1 (MEN1), von Hippel-Lindau disease (VHL), neurofibromatosis type 1 and tuberous sclerosis) that are all inherited as autosomal dominant traits and result from mutations of tumour suppressor genes.
  • Tumours of the endocrine pancreas develop in 30-80% of patients carrying mutations of the MEN1 gene.
  • Tumours of the endocrine pancreas are infrequent in patients suffering from VHL, neurofibromatosis and tuberous sclerosis.
  • In this review article, the authors present a synopsis of tumours of the endocrine pancreas related to these hereditary syndromes underlining the clinical characteristics, diagnostical and therapeutical possibilities.
  • [MeSH-major] Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Gastrinoma / diagnosis. Gastrinoma / genetics. Glucagonoma / genetics. Humans. Insulinoma / diagnosis. Insulinoma / genetics. Mass Screening. Multiple Endocrine Neoplasia Type 1 / complications. Neurofibromatosis 1 / complications. Somatostatinoma / genetics. Tuberous Sclerosis / complications. Vipoma / genetics. von Hippel-Lindau Disease / complications

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  • (PMID = 16509219.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 50
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5. Serafimidis I, Rakatzi I, Episkopou V, Gouti M, Gavalas A: Novel effectors of directed and Ngn3-mediated differentiation of mouse embryonic stem cells into endocrine pancreas progenitors. Stem Cells; 2008 Jan;26(1):3-16
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  • [Title] Novel effectors of directed and Ngn3-mediated differentiation of mouse embryonic stem cells into endocrine pancreas progenitors.
  • The delineation of regulatory networks involved in early endocrine pancreas specification will play a crucial role in directing the differentiation of embryonic stem cells toward the mature phenotype of beta cells for cell therapy of type 1 diabetes.
  • The transcription factor Ngn3 is required for the specification of the endocrine lineage, but its direct targets and the scope of biological processes it regulates remain elusive.
  • Microarray gene expression profiling at distinct time points following Ngn3 induction suggested novel and diverse roles of Ngn3 in pancreas endocrine cell specification.
  • Furthermore, the combination of in vivo patterning signals and inducible Ngn3 expression enhances ESC differentiation toward the pancreas endocrine lineage.
  • This is shown by strong upregulation of endocrine lineage terminal differentiation markers and strong expression of the hormones glucagon, somatostatin, and insulin.
  • These data suggest that bona fide pancreas endocrine cells have been generated and that timely induction of Ngn3 expression can play a decisive role in directing ESC differentiation toward the endocrine lineage.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Differentiation / physiology. Embryonic Stem Cells / cytology. Islets of Langerhans / embryology. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism

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  • (PMID = 17932425.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U120074332
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / Nerve Tissue Proteins; 0 / Neurog3 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein; 0 / transcription factor PTF1
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6. Itkin-Ansari P, Marcora E, Geron I, Tyrberg B, Demeterco C, Hao E, Padilla C, Ratineau C, Leiter A, Lee JE, Levine F: NeuroD1 in the endocrine pancreas: localization and dual function as an activator and repressor. Dev Dyn; 2005 Jul;233(3):946-53
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  • [Title] NeuroD1 in the endocrine pancreas: localization and dual function as an activator and repressor.
  • The basic helix-loop-helix transcription factor NeuroD1 regulates cell fate in the nervous system but previously has not been considered to function similarly in the endocrine pancreas due to its reported expression in all islet cell types in the newborn mouse.
  • Consistent with a previous report, NeuroD1 colocalizes with glucagon as well as insulin in immature islets of the newborn mouse.
  • Transfection studies using insulin and somatostatin promoters confirm the ability of NeuroD1 to act as both a transcriptional repressor and activator in the same cell, suggesting a more complex role for NeuroD1 in the establishment and/or maintenance of mature endocrine cells than has been recognized previously.
  • [MeSH-major] Gene Expression Profiling. Nerve Tissue Proteins / metabolism. Pancreas / metabolism. Pancreas / secretion. Repressor Proteins / metabolism. Trans-Activators / metabolism
  • [MeSH-minor] Aging / physiology. Amyloid / metabolism. Animals. Animals, Newborn. Basic Helix-Loop-Helix Transcription Factors. Cell Line. DNA / metabolism. DNA-Binding Proteins / chemistry. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Insulin / genetics. Islets of Langerhans / cytology. Islets of Langerhans / metabolism. Mice. Promoter Regions, Genetic / genetics. Protein Structure, Tertiary. Somatostatin / genetics. Somatostatin / metabolism. Transcription Factors / metabolism. Transcription, Genetic / genetics

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  • (PMID = 15906379.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 55065; United States / NIDDK NIH HHS / DK / DK34928; United States / NIDDK NIH HHS / DK / DK43673; United States / NIDDK NIH HHS / DK / DK52870; United States / NIDDK NIH HHS / DK / DK55283; United States / NIDDK NIH HHS / DK / DK61248
  • [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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Nerve Tissue Proteins; 0 / Nkx-2.2 homedomain protein; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein; 169238-82-8 / NeuroD protein; 51110-01-1 / Somatostatin; 9007-49-2 / DNA
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7. Chuang JC, Cha JY, Garmey JC, Mirmira RG, Repa JJ: Research resource: nuclear hormone receptor expression in the endocrine pancreas. Mol Endocrinol; 2008 Oct;22(10):2353-63
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  • [Title] Research resource: nuclear hormone receptor expression in the endocrine pancreas.
  • The endocrine pancreas comprises the islets of Langerhans, tiny clusters of cells that contribute only about 2% to the total pancreas mass.
  • However, this little endocrine organ plays a critical role in maintaining glucose homeostasis by the regulated secretion of insulin (by beta-cells) and glucagon (by alpha-cells).
  • As a first step in addressing potential roles of peroxisome proliferator-activated receptor-gamma and other nuclear hormone receptors (NHRs) in the biology of the endocrine pancreas, we have used quantitative real-time PCR to profile the expression of all 49 members of the mouse NHR superfamily in primary islets, and cell lines that represent alpha-cells (alphaTC1) and beta-cells (betaTC6 and MIN6).
  • In summary, 19 NHR members were highly expressed in both alpha- and beta-cell lines, 13 receptors showed predominant expression (at least an 8-fold difference) in alpha- vs. beta-cell lines, and 10 NHRs were not expressed in the endocrine pancreas.
  • In addition we evaluated the relative expression of these transcription factors during hyperglycemia and found that 16 NHRs showed significantly altered mRNA levels in mouse islets.
  • A similar survey was conducted in primary human islets to reveal several significant differences in NHR expression between mouse and man.
  • These data identify potential therapeutic targets in the endocrine pancreas for the treatment of diabetes mellitus.

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  • (PMID = 18669644.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK060581; United States / NIDDK NIH HHS / DK / R01 DK60581
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2582538
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8. Remacle C, Dumortier O, Bol V, Goosse K, Romanus P, Theys N, Bouckenooghe T, Reusens B: Intrauterine programming of the endocrine pancreas. Diabetes Obes Metab; 2007 Nov;9 Suppl 2:196-209
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intrauterine programming of the endocrine pancreas.
  • Animal models have been established and studies have demonstrated that reduction in the availability of nutrients during foetal development programs the endocrine pancreas and insulin-sensitive tissues.
  • [MeSH-major] Diabetes Mellitus / embryology. Pancreas / embryology. Pancreatic Diseases / embryology

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  • (PMID = 17919194.001).
  • [ISSN] 1462-8902
  • [Journal-full-title] Diabetes, obesity & metabolism
  • [ISO-abbreviation] Diabetes Obes Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 117
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9. Reusens B, Remacle C: Programming of the endocrine pancreas by the early nutritional environment. Int J Biochem Cell Biol; 2006;38(5-6):913-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Programming of the endocrine pancreas by the early nutritional environment.
  • It focuses on the alteration of the endocrine pancreas at birth.
  • [MeSH-major] Pancreas / embryology. Prenatal Exposure Delayed Effects
  • [MeSH-minor] Animals. Diabetes, Gestational / physiopathology. Female. Humans. Insulin-Secreting Cells / pathology. Islets of Langerhans / embryology. Mitochondria / physiology. Pregnancy. Protein Deficiency / complications. Protein-Energy Malnutrition / complications. Uterus / blood supply

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  • (PMID = 16337425.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 66
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10. Malaisse WJ: Non-invasive imaging of the endocrine pancreas (review). Int J Mol Med; 2005 Feb;15(2):243-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-invasive imaging of the endocrine pancreas (review).
  • The non-invasive imaging of the endocrine pancreas is currently considered by concerned institutions as a priority theme of research.
  • Because the endocrine pancreas represents only about one percent of the pancreatic gland, highly specific tools are required for labelling the insulin-producing cells.
  • The present review deals with the possible use of D-mannoheptulose for the non-invasive quantification of insulin-producing cells in the pancreas.
  • These metabolites remain in the islet cells after prolonged washing, suggesting that imaging of the pancreas at a relatively late time after intravenous administration of D-mannoheptulose could avoid significant extracellular contamination.
  • Using tritiated D-mannoheptulose as tracer, a new method was designed for quantification of the total mass of insulin-producing cells in either isolated perfused rat pancreata or isolated pancreatic islets.
  • In the light of results obtained with 6-deoxy-6-iodo-D-glucose, it is proposed that 7-deoxy-7-iodo-D-mannoheptulose could be used for the non-invasive imaging of the endocrine pancreas.
  • [MeSH-major] Diagnostic Imaging / methods. Pancreas / pathology
  • [MeSH-minor] Animals. Glucose Transporter Type 2. Hepatocytes / metabolism. Humans. Insulin / metabolism. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Mannoheptulose / metabolism. Models, Biological. Monosaccharide Transport Proteins / metabolism. Rats

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  • (PMID = 15647838.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Glucose Transporter Type 2; 0 / Insulin; 0 / Monosaccharide Transport Proteins; 654-29-5 / Mannoheptulose
  • [Number-of-references] 30
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11. Hanazaki K, Maeda H, Okabayashi T: Tight perioperative glycemic control using an artificial endocrine pancreas. Surg Today; 2010;40(1):1-7
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  • [Title] Tight perioperative glycemic control using an artificial endocrine pancreas.
  • Van den Berghe et al. reported in 2001 that tight glycemic control (maintaining blood glucose levels at 80-110 mg/dl) improved morbidity and mortality in the surgical intensive care unit.
  • We recently demonstrated that achieving perioperative tight glycemic control using an artificial endocrine pancreas for surgical patients was a safe and effective method for decreasing the incidence of POI without increasing the risk of hypoglycemia.
  • Strict perioperative glycemic control using a closed-loop artificial endocrine pancreas system is recommended for safe and effective performance of IIT.
  • [MeSH-major] Hyperglycemia / prevention & control. Infection Control / methods. Pancreas, Artificial. Perioperative Care. Postoperative Complications / prevention & control
  • [MeSH-minor] Animals. Blood Glucose / analysis. Critical Illness. Diabetes Complications / prevention & control. Humans. Hypoglycemic Agents / therapeutic use. Insulin / therapeutic use. Islets of Langerhans / metabolism. Time Factors

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  • (PMID = 20037833.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Hypoglycemic Agents; 0 / Insulin
  • [Number-of-references] 43
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12. Kim HJ, Sumanas S, Palencia-Desai S, Dong Y, Chen JN, Lin S: Genetic analysis of early endocrine pancreas formation in zebrafish. Mol Endocrinol; 2006 Jan;20(1):194-203
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic analysis of early endocrine pancreas formation in zebrafish.
  • Endocrine pancreas of zebrafish consist of at least four different cell types that function similarly to mammalian pancreatic islet.
  • No mutants specifically affecting formation of the endocrine pancreas have been identified during the previous large-scale mutagenesis screens in zebrafish due to invisibility of a pancreatic islet.
  • These data indicate that there are separate mechanisms regulating endocrine cell migration, proliferation, and differentiation.
  • [MeSH-major] Insulin / metabolism. Pancreas / embryology. Zebrafish / embryology. Zebrafish / genetics
  • [MeSH-minor] Animals. Glucagon / metabolism. In Situ Hybridization. Islets of Langerhans / cytology. Islets of Langerhans / embryology. Morphogenesis. Mutagenesis. Mutation. Phenotype

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  • (PMID = 16099813.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01HD041367; United States / NIEHS NIH HHS / ES / R21ES012990; United States / NIGMS NIH HHS / GM / T32-GM008244
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 9007-92-5 / Glucagon
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13. Trucco M: Is Facilitating Pancreatic Beta Cell Regeneration a Valid Option for Clinical Therapy? Cell Transplant; 2006 Jan;15(1_suppl):75-84

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There is accumulating evidence that the endocrine pancreas has regenerative properties, that hematopoietic chimerism can abrogate destruction of beta cells in autoimmune diabetes, and that, in this manner, physiologically sufficient endogenous insulin production can be restored in clinically diabetic NOD mice.

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  • (PMID = 28863766.001).
  • [ISSN] 1555-3892
  • [Journal-full-title] Cell transplantation
  • [ISO-abbreviation] Cell Transplant
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Autoimmunity / Beta cell precursors / Beta cell regeneration / Tolerization / Type 1 diabetes
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14. Gromada J, Franklin I, Wollheim CB: α-Cells of the Endocrine Pancreas: 35 Years of Research but the Enigma Remains. Endocr Rev; 2007 Feb 01;28(1):84-116

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] α-Cells of the Endocrine Pancreas: 35 Years of Research but the Enigma Remains.

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  • (PMID = 28199574.001).
  • [ISSN] 1945-7189
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Morimoto S, Morales A, Zambrano E, Fernandez-Mejia C: Sex steroids effects on the endocrine pancreas. J Steroid Biochem Mol Biol; 2010 Oct;122(4):107-13

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sex steroids effects on the endocrine pancreas.
  • The endocrine pancreas is central in the physiopathology of diabetes mellitus.
  • Nutrients and hormones control endocrine pancreatic function and the secretion of insulin and other pancreatic islet hormones.
  • Although the pancreas is not usually considered as a target of steroids, increasing evidence indicates that sex steroid hormones modify pancreatic islet function.
  • In this review, we focused on the effects of sex steroid hormones on endocrine pancreatic function, with special emphasis in animal studies.
  • [MeSH-major] Gonadal Steroid Hormones / metabolism. Islets of Langerhans / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20580673.001).
  • [ISSN] 1879-1220
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones
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16. Ropero AB, Alonso-Magdalena P, García-García E, Ripoll C, Fuentes E, Nadal A: Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis. Int J Androl; 2008 Apr;31(2):194-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis.
  • The link between endocrine disruptors and altered blood glucose homeostasis has been recently suggested.
  • Environmentally relevant doses of the ubiquitous endocrine disruptor bisphenol-A (BPA) have profound effects on mice endocrine pancreas--an essential tissue involved in glucose metabolism.
  • BPA exerts rapid non-genomic effects on insulin releasing beta-cells and glucagon releasing alpha-cells within freshly isolated islets of Langerhans.
  • [MeSH-major] Blood Glucose / metabolism. Endocrine Disruptors / toxicity. Homeostasis. Pancreas / drug effects. Phenols / toxicity

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  • (PMID = 17971160.001).
  • [ISSN] 1365-2605
  • [Journal-full-title] International journal of andrology
  • [ISO-abbreviation] Int. J. Androl.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzhydryl Compounds; 0 / Blood Glucose; 0 / Endocrine Disruptors; 0 / Phenols; MLT3645I99 / bisphenol A
  • [Number-of-references] 30
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17. Kann PH, Meyer S, Zielke A, Langer P, Ivan D: [The new role for endoscopic ultrasound in endocrinology: imaging of the adrenals and the endocrine pancreas]. Dtsch Med Wochenschr; 2006 Mar 17;131(11):567-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The new role for endoscopic ultrasound in endocrinology: imaging of the adrenals and the endocrine pancreas].
  • [Transliterated title] Die neue Rolle der Endosonographie in der Endokrinologie: Bildgebung der Nebennieren und des endokrinen Pankreas.
  • Endoscopic ultrasound imaging of the adrenals and the endocrine pancreas enriches the diagnostic repertoire and improves the clinical opportunities of endocrinology.
  • Endoscopic ultrasound imaging is especially relevant in the diagnosis of insulinomas and primary hyperaldosteronism, because it has direct consequences in planning a diagnostic and therapeutic strategy.
  • [MeSH-major] Adrenal Gland Diseases / ultrasonography. Adrenal Glands / ultrasonography. Endosonography / methods. Pancreas / ultrasonography. Pancreatic Diseases / ultrasonography
  • [MeSH-minor] Diagnosis, Differential. Humans

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  • (PMID = 16538563.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 23
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18. Jain R, Lammert E: Cell-cell interactions in the endocrine pancreas. Diabetes Obes Metab; 2009 Nov;11 Suppl 4:159-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell-cell interactions in the endocrine pancreas.
  • The islets of Langerhans forming the endocrine pancreas are composed of alpha-, beta-, delta-, epsilon- and PP-cells, and interactions between these cells are required for fine-tuning glucose homeostasis of the body.
  • The endocrine cells communicate through homotypic or heterotypic cell-cell adhesion, or in a paracrine fashion, and this communication is involved in the regulated secretion of islet hormones.
  • This review discusses how islet hormones, secreted molecules and ions influence the endocrine cells and how cell adhesion molecules such as neural cell adhesion molecule, cadherins, connexin-36, Eph receptors and ephrin ligands, as well as extracellular matrix proteins, modulate pancreatic islet function.
  • [MeSH-major] Cell Communication / physiology. Insulin-Secreting Cells / physiology. Islets of Langerhans / cytology. Neural Cell Adhesion Molecules / physiology. Receptors, Eph Family / physiology

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  • (PMID = 19817798.001).
  • [ISSN] 1463-1326
  • [Journal-full-title] Diabetes, obesity & metabolism
  • [ISO-abbreviation] Diabetes Obes Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; EC 2.7.10.1 / Receptors, Eph Family
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19. Ballian N, Brunicardi FC, Wang XP: Somatostatin and its receptors in the development of the endocrine pancreas. Pancreas; 2006 Jul;33(1):1-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin and its receptors in the development of the endocrine pancreas.
  • The development of the endocrine pancreas is regulated by numerous transcription and growth factors.
  • Somatostatin (SST) is present in many tissues and acts as a neurotransmitter and autocrine/paracrine/endocrine regulator in response to ions, nutrients, peptides, and hormones as well as neurotransmitters.
  • In the pancreas, there is evidence that SST acts an inhibitory paracrine regulator of hormone secretion.
  • Interactions of SST and SSTRs are not only important during normal pancreas development, but have also been implicated in many pancreatic diseases such as diabetes mellitus and pancreatic cancer.
  • In this review article, we use evidence from recently published animal studies to present the critical roles of SST and SSTRs proteins in the development of the endocrine pancreas.
  • [MeSH-major] Islets of Langerhans / metabolism. Receptors, Somatostatin / metabolism. Somatostatin / metabolism

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  • (PMID = 16804406.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Receptors, Somatostatin; 0 / Transcription Factors; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 51110-01-1 / Somatostatin
  • [Number-of-references] 172
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20. Rozzo A, Meneghel-Rozzo T, Delakorda SL, Yang SB, Rupnik M: Exocytosis of insulin: in vivo maturation of mouse endocrine pancreas. Ann N Y Acad Sci; 2009 Jan;1152:53-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exocytosis of insulin: in vivo maturation of mouse endocrine pancreas.
  • In order to work with embryonic and newborn endocrine pancreas, we used organotypic slices.
  • The mouse embryonic pancreas slices show high basal insulin release that is not further elevated by high glucose levels.
  • [MeSH-major] Exocytosis. Insulin / secretion. Islets of Langerhans / secretion

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  • (PMID = 19161376.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Insulin; 0 / Potassium Channels; IY9XDZ35W2 / Glucose
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21. Strowski MZ, Blake AD: Function and expression of somatostatin receptors of the endocrine pancreas. Mol Cell Endocrinol; 2008 May 14;286(1-2):169-79
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Function and expression of somatostatin receptors of the endocrine pancreas.
  • In the pancreas, SST is a potent regulator of insulin and glucagon secretion.
  • By combining the results obtained from molecular biology, pharmacology and immunochemical studies the current review provides a summary of important recent developments which have extended our knowledge of SST actions in the endocrine pancreas.
  • [MeSH-major] Islets of Langerhans / metabolism. Receptors, Somatostatin / metabolism. Somatostatin / metabolism

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  • (PMID = 18375050.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 58
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22. Bertelli E, Bendayan M: Association between endocrine pancreas and ductal system. More than an epiphenomenon of endocrine differentiation and development? J Histochem Cytochem; 2005 Sep;53(9):1071-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association between endocrine pancreas and ductal system. More than an epiphenomenon of endocrine differentiation and development?
  • Traditional histological descriptions of the pancreas distinguish between the exocrine and the endocrine pancreas, as if they were two functionally distinct glands.
  • Less attention, however, has traditionally been paid to the relationships occurring between the endocrine pancreas and the ductal system.
  • Associations between islet tissue and ducts are considered by most researchers as only a transient epiphenomenon of endocrine development.
  • The pancreas appears at present to be an integrated organ composed of three functionally related components of well-orchestrated endocrine and exocrine physiological responses.
  • [MeSH-major] Islets of Langerhans / anatomy & histology. Islets of Langerhans / physiology. Pancreatic Ducts / anatomy & histology. Pancreatic Ducts / physiology
  • [MeSH-minor] Animals. Humans. Pancreas, Exocrine / anatomy & histology. Pancreas, Exocrine / physiology. Pancreas, Exocrine / secretion. Pancreatic Hormones / secretion

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  • (PMID = 15956021.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pancreatic Hormones
  • [Number-of-references] 203
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23. Gromada J, Franklin I, Wollheim CB: Alpha-cells of the endocrine pancreas: 35 years of research but the enigma remains. Endocr Rev; 2007 Feb;28(1):84-116
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-cells of the endocrine pancreas: 35 years of research but the enigma remains.
  • Glucagon, a hormone secreted from the alpha-cells of the endocrine pancreas, is critical for blood glucose homeostasis.
  • The control of glucagon secretion is multifactorial and involves direct effects of nutrients on alpha-cell stimulus-secretion coupling as well as paracrine regulation by insulin and zinc and other factors secreted from neighboring beta- and delta-cells within the islet of Langerhans.

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  • (PMID = 17261637.001).
  • [ISSN] 0163-769X
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 433
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24. May CL: The role of Islet-1 in the endocrine pancreas: Lessons from pancreas specific Islet-1 deficient mice. Islets; 2010 Mar-Apr;2(2):121-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of Islet-1 in the endocrine pancreas: Lessons from pancreas specific Islet-1 deficient mice.
  • Recently, we have reported the LIM-homeodoman (HD) transcriptional regulator, Islet-1 (Isl-1) as a key regulator for pancreatic islets after the secondary transition and into early postnatal stages in mice.
  • Previously, the role of Isl-1 had only been examined during early pancreas development in vivo and cell lines.
  • These early studies concluded that Isl-1 is required for the differentiation of early endocrine cells, and hormone gene expression is regulated by Isl-1 in cell culture.
  • In addition, the function of Isl-1 during the formation of principle hormone producing endocrine cells had not been investigated since Isl-1 null animals die prior to the formation of these cells.
  • Using pancreas-specific inactivation of Isl-1 in mice, we have elucidated the role of Isl-1 during maturation, proliferation and survival of the endocrine pancreas after the secondary transition.

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  • (PMID = 21099304.001).
  • [ISSN] 1938-2022
  • [Journal-full-title] Islets
  • [ISO-abbreviation] Islets
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK078606-03; United States / NIDDK NIH HHS / DK / DK078606-03; United States / NIDDK NIH HHS / DK / P30-DK19525; United States / NIDDK NIH HHS / DK / DK019525; United States / NIDDK NIH HHS / DK / P30-DK050306; United States / NIDDK NIH HHS / DK / DK078606; United States / NIDDK NIH HHS / DK / R01 DK078606
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / LIM-Homeodomain Proteins; 0 / Maf Transcription Factors, Large; 0 / Mafa protein, mouse; 0 / Transcription Factors; 0 / insulin gene enhancer binding protein Isl-1
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25. Granata R, Baragli A, Settanni F, Scarlatti F, Ghigo E: Unraveling the role of the ghrelin gene peptides in the endocrine pancreas. J Mol Endocrinol; 2010 Sep;45(3):107-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unraveling the role of the ghrelin gene peptides in the endocrine pancreas.
  • The endocrine pancreas is necessary for glucose homeostasis maintenance.
  • AG, UAG, and Ob are expressed in both human and rodent pancreatic islets from fetal to adult life, and the pancreas is the major source of ghrelin in the perinatal period.
  • GHS-R1a and GPR39 expression has been shown in beta-cells and islets, as well as specific binding sites for AG, UAG, and Ob.
  • Indeed, AG, UAG, and Ob regulate insulin secretion in beta-cells and isolated islets, promote beta-cell proliferation and survival, inhibit beta-cell and human islet cell apoptosis, and modulate the expression of genes that are essential in pancreatic islet cell biology.
  • The present review summarizes the newest findings on AG, UAG, and Ob expression in pancreatic islets and the role of these peptides on beta-cell development, survival, and function.
  • [MeSH-major] Ghrelin / genetics. Ghrelin / metabolism. Islets of Langerhans / metabolism

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  • (PMID = 20595321.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Insulin
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26. Fjällskog ML, Hessman O, Eriksson B, Janson ET: Upregulated expression of PDGF receptor beta in endocrine pancreatic tumors and metastases compared to normal endocrine pancreas. Acta Oncol; 2007;46(6):741-6
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  • [Title] Upregulated expression of PDGF receptor beta in endocrine pancreatic tumors and metastases compared to normal endocrine pancreas.
  • Platelet-derived growth factor receptor (PDGFR) beta signaling is involved in autocrine growth stimulation of tumor cells, tumor angiogenesis and regulation of tumor interstitial fluid pressure.
  • Malignant endocrine pancreatic tumors (EPTs) express PDGFR beta both in stroma and on tumor cells.
  • To investigate the role of PDGFR beta signaling in EPTs we compared PDGFR beta expression in normal endocrine pancreas to malignant EPTs and metastases.
  • PDGFR beta expression was examined by immunohistochemistry using specific polyclonal antibodies in ten tissue samples from normal endocrine pancreas, 21 from primary EPTs and 19 from metastases.
  • In eight patients we compared the expression in normal endocrine pancreas to the corresponding primary tumor and metastases, in two patients normal tissue to the primary tumor and in 11 patients primary tumors to the corresponding metastases.
  • Six of ten tissues containing normal pancreas stained negative for PDGFR beta on endocrine cells, while seven of ten stained positive in the stroma.
  • Eighteen of 21 (86%) primary tumors stained positive for PDGFR beta on tumor cells and all had positive stroma stainings.
  • All 19 metastases stained positive for PDGFR beta on tumor cells and in evaluable stroma (n=16).
  • We have found that PDGFR beta is more frequently expressed in primary EPTs and metastases as compared to normal endocrine pancreatic tissue.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Endocrine System / physiopathology. Endocrine System Diseases / physiopathology. Pancreas / physiopathology. Pancreatic Neoplasms / physiopathology. Receptor, Platelet-Derived Growth Factor beta / physiology

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  • (PMID = 17653895.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
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27. Youson JH, Al-Mahrouki AA, Amemiya Y, Graham LC, Montpetit CJ, Irwin DM: The fish endocrine pancreas: review, new data, and future research directions in ontogeny and phylogeny. Gen Comp Endocrinol; 2006 Sep 1;148(2):105-15
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  • [Title] The fish endocrine pancreas: review, new data, and future research directions in ontogeny and phylogeny.
  • The literature on the ontogeny and phylogeny of the endocrine pancreas of ray-finned fishes is summarized since the latest review in fish [Youson, J.H., Al-Mahrouki, A.A., 1999. Review.
  • Ontogenetic and phylogenetic development of the endocrine pancreas (islet organ) in fishes. Gen. Comp. Endocrinol.
  • The present study also provides the first comparative analysis of sequences of preprohormones of endocrine peptides from closely related basal teleost species.
  • [MeSH-major] Fishes / embryology. Fishes / genetics. Fishes / physiology. Islets of Langerhans / embryology. Islets of Langerhans / physiology

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  • (PMID = 16430894.001).
  • [ISSN] 0016-6480
  • [Journal-full-title] General and comparative endocrinology
  • [ISO-abbreviation] Gen. Comp. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 51110-01-1 / Somatostatin; 59763-91-6 / Pancreatic Polypeptide
  • [Number-of-references] 58
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28. Paolucci M, Buono S, Sciarrillo R, Putti R: Effects of leptin administration on the endocrine pancreas and liver in the lizard Podarcis sicula. J Exp Zool A Comp Exp Biol; 2006 May 1;305(5):383-95
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  • [Title] Effects of leptin administration on the endocrine pancreas and liver in the lizard Podarcis sicula.
  • In this study, we investigated the presence of leptin receptor in pancreatic islets and the effect of exogenous leptin administration in Podarcis sicula on glucose metabolism.
  • Our data show the presence of leptin receptor immunoreactivity in the endocrine pancreas suggesting that leptin may act at a peripheral level as previously postulated in mammals.
  • [MeSH-major] Islets of Langerhans / drug effects. Leptin / pharmacology. Liver / drug effects. Lizards / physiology

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  • (PMID = 16526046.001).
  • [ISSN] 1548-8969
  • [Journal-full-title] Journal of experimental zoology. Part A, Comparative experimental biology
  • [ISO-abbreviation] J. Exp. Zoolog. Part A Comp. Exp. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Leptin; 0 / Liver Extracts; 0 / Receptors, Cell Surface; 0 / Receptors, Leptin; 0 / leptin receptor, mouse; 9007-92-5 / Glucagon
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29. Bradley SP, Rastellini C, da Costa MA, Kowalik TF, Bloomenthal AB, Brown M, Cicalese L, Basadonna GP, Uknis ME: Gene silencing in the endocrine pancreas mediated by short-interfering RNA. Pancreas; 2005 Nov;31(4):373-9
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  • [Title] Gene silencing in the endocrine pancreas mediated by short-interfering RNA.
  • OBJECTIVES: RNA interference as mediated by short-interfering RNA (siRNA) offers a nonviral means to silence genes in tissue; however, few data exist about gene therapy using siRNA in pancreas tissue.
  • To determine if siRNA treatment could silence an endogenous gene in pancreatic islets, we developed a murine model using the endocrine pancreas.
  • Isolated pancreatic islets were transfected with siRNA in vitro using a liposomal delivery method in a dose titration (50-400 nM) or pooled from BALB/c mice having received siRNA (100 microg) via hydrodynamic tail vein injection.
  • In vivo delivery of siRNA to pancreatic islets revealed a 33% reduction in Ins2 mRNA levels, although siRNA was able to be detected in 19% of isolated islet cells.
  • CONCLUSION: We have successfully used RNA interference to silence an endogenous tissue-specific gene (Ins2) in pancreatic islets when transfected in vitro or administered in vivo.
  • [MeSH-major] Gene Silencing. Islets of Langerhans / metabolism. RNA, Small Interfering / pharmacology

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  • (PMID = 16258373.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 0 / RNA, Small Interfering
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30. Tikellis C, Cooper ME, Thomas MC: Role of the renin-angiotensin system in the endocrine pancreas: implications for the development of diabetes. Int J Biochem Cell Biol; 2006;38(5-6):737-51
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  • [Title] Role of the renin-angiotensin system in the endocrine pancreas: implications for the development of diabetes.
  • In the endocrine pancreas, all the components of an active renin-angiotensin system are present, which modulate a range of activities including local blood flow, hormone release and prostaglandin synthesis.
  • In both types 1 and 2 diabetes, there is an up-regulation of its expression and activity in the endocrine pancreas.
  • Moreover, the incidence of de novo diabetes appears to be significantly reduced by blockade of the renin-angiotensin system in clinical studies.
  • [MeSH-major] Diabetes Mellitus / etiology. Pancreas / physiology. Renin-Angiotensin System / physiology
  • [MeSH-minor] Angiotensin I / physiology. Angiotensin II / physiology. Angiotensinogen / biosynthesis. Animals. Diabetes Mellitus, Type 1 / physiopathology. Diabetes Mellitus, Type 2 / etiology. Fibrosis. Humans. Hyperglycemia / complications. Hyperglycemia / physiopathology. Hypoglycemia / chemically induced. Islets of Langerhans / pathology. PPAR gamma / physiology. Peptidyl-Dipeptidase A / biosynthesis. Receptors, Angiotensin / biosynthesis. Renin / biosynthesis

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  • (PMID = 16198140.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Receptors, Angiotensin; 11002-13-4 / Angiotensinogen; 11128-99-7 / Angiotensin II; 9041-90-1 / Angiotensin I; EC 3.4.15.1 / Peptidyl-Dipeptidase A; EC 3.4.23.15 / Renin
  • [Number-of-references] 131
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31. Maeda H, Okabayashi T, Yatabe T, Yamashita K, Hanazaki K: Perioperative intensive insulin therapy using artificial endocrine pancreas in patients undergoing pancreatectomy. World J Gastroenterol; 2009 Sep 7;15(33):4111-5
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  • [Title] Perioperative intensive insulin therapy using artificial endocrine pancreas in patients undergoing pancreatectomy.
  • This review discusses the endocrine aspects of pancreatic resection and highlights postoperative glycemic control using a closed-loop system or artificial pancreas.
  • In previous experiments, we have demonstrated the reliability of the artificial pancreas in dogs with total pancreatectomy, and its postoperative clinical use has been shown to be effective and safe, without the occurrence of hypoglycemic episodes, even in patients after total pancreatectomy.
  • Considering the increasing requirement for tight perioperative glycemic control and the recognized risk of hypoglycemia, we propose the use of an artificial endocrine pancreas that is able to monitor continuously blood glucose concentrations with proven accuracy, and administer automatically substances to return blood glucose concentration to the optimal narrow range.

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  • (PMID = 19725142.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Blood Glucose; 59763-91-6 / Pancreatic Polypeptide; 9007-92-5 / Glucagon
  • [Number-of-references] 38
  • [Other-IDs] NLM/ PMC2738804
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32. Shanmugam C, Katkoori VR, Jhala NC, Grizzle WE, Manne U: Immunohistochemical expression of rabphilin-3A-like (Noc2) in normal and tumor tissues of human endocrine pancreas. Biotech Histochem; 2009 Apr;84(2):39-45
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  • [Title] Immunohistochemical expression of rabphilin-3A-like (Noc2) in normal and tumor tissues of human endocrine pancreas.
  • Involvement of rabphilin-3A-like (RPH3AL), or Noc2, the potential effector of Ras-associated binding proteins Rab3A and Rab27A in the regulation of exocytotic processes in the endocrine pancreas has been demonstrated in experimental models.
  • We evaluated immunohistochemical expression of the key molecules of the exocytotic machinery, Noc2, Rab3A, Rab27A, and RIM2, together with the characteristic islet cell hormones, insulin and glucagon in normal and endocrine tumor tissues of human pancreas.
  • Normal pancreatic islets were stained for all of these proteins and showed strong cytoplasmic localization.
  • A similar pattern of strong cytoplasmic expression of these proteins was observed in the majority of endocrine tumors.
  • By contrast, the exocrine portions of normal appearing pancreas completely lacked Rab27A staining and showed decreased expression of the proteins, Noc2, Rab3A, and RIM2.
  • The staining pattern of Noc2 and Rab27A was similar to the staining pattern of glucagon-producing cells within the islets.
  • The concomitant expression of Noc2 with these molecules suggests that Noc2 may serve as an effector for Rab3A and Rab27A and that it is involved in the regulation of exocytosis of the endocrine pancreas in humans.
  • [MeSH-major] Pancreas / metabolism. Pancreatic Neoplasms / chemistry. rab GTP-Binding Proteins / analysis

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  • (PMID = 19212825.001).
  • [ISSN] 1473-7760
  • [Journal-full-title] Biotechnic & histochemistry : official publication of the Biological Stain Commission
  • [ISO-abbreviation] Biotech Histochem
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098932-05; United States / NCI NIH HHS / CA / P20CA101955-05; United States / NCI NIH HHS / CA / P20 CA101955; United States / NCI NIH HHS / CA / U54 CA118623; United States / NCI NIH HHS / CA / U54 CA118948; United States / NCI NIH HHS / CA / R01 CA098932; United States / NCI NIH HHS / CA / U24-CA086359; United States / NCI NIH HHS / CA / R01-CA98932-01; United States / NCI NIH HHS / CA / U24 CA086359; United States / NCI NIH HHS / CA / U54-CA118948
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RPH3AL protein, human; EC 3.6.5.2 / rab GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS100642; NLM/ PMC2667687
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33. Wang XP, Norman M, Yang J, Liu SH, Magnusson J, DeMayo FJ, Brunicardi FC: The effect of global SSTR5 gene ablation on the endocrine pancreas and glucose regulation in aging mice. J Surg Res; 2005 Nov;129(1):64-72
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  • [Title] The effect of global SSTR5 gene ablation on the endocrine pancreas and glucose regulation in aging mice.
  • INTRODUCTION: The purpose of this study was to examine the effect of global gene ablation of SSTR5 on the endocrine pancreas, insulin secretion, and glucose tolerance in aging mice, as SSTR5 is a primary regulator of insulin secretion in the mouse pancreas.
  • Basal and glucose-stimulated insulin secretion in vitro was studied using the isolated perfused mouse pancreas model at 3 and 12 months.
  • IPGTT demonstrated that 3-month-old SSTR5-/- mice were glucose intolerant despite similar insulin secretion both in vivo and in vitro and enlarged islets.
  • At 12 months of age, SSTR5-/- mice had basal hypoglycemia and improved glucose intolerance associated with hyperinsulinemia in vivo and in vitro and enlarged islets.
  • SSTR1 expression was significantly increased in islets at 3 months of age, but was nearly absent in islets at 12 months of age, as was somatostatin staining in SSTR5-/- mice.
  • [MeSH-major] Aging. Glucose / pharmacology. Insulin / secretion. Islets of Langerhans / secretion. Receptors, Somatostatin / deficiency. Receptors, Somatostatin / genetics

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  • (PMID = 16026801.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01-DK46441
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5; 9007-92-5 / Glucagon; IY9XDZ35W2 / Glucose
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34. Jackerott M, Lee YC, Møllgård K, Kofod H, Jensen J, Rohleder S, Neubauer N, Gaarn LW, Lykke J, Dodge R, Dalgaard LT, Søstrup B, Jensen DB, Thim L, Nexø E, Thams P, Bisgaard HC, Nielsen JH: Trefoil factors are expressed in human and rat endocrine pancreas: differential regulation by growth hormone. Endocrinology; 2006 Dec;147(12):5752-9
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  • [Title] Trefoil factors are expressed in human and rat endocrine pancreas: differential regulation by growth hormone.
  • Because pancreas developmentally arises from the primitive foregut, we explored the expression of TFFs in the pancreas in man and rat.
  • Immunocytochemical staining of adult human pancreas showed abundant TFF3 immunoreactivity in pancreatic islets and some duct cells, whereas weak TFF1 and no TFF2 staining were detected.
  • In the islets TFF3 localized to most insulin and some glucagon and pancreatic polypeptide-producing cells.
  • TFF3 immunoreactivity was colocalized with insulin and glucagon in distinct cell clusters in human fetal pancreas at wk 14 and in the newborn rat pancreas.
  • In isolated human and rat islets, TFF3 and TFF1 mRNA was identified by RT-PCR, and TFF3 protein was detected in human pancreas and islets by ELISA.
  • Exposure of neonatal rat islets or insulinoma cells to GH, a known beta-cell growth factor, resulted in markedly increased TFF3 but decreased TFF1 mRNA levels.
  • Culture of neonatal rat islets in the presence of TFF3 resulted in attachment and migration of the islet cells, but no effects on proliferation, insulin secretion or cytokine-induced apoptosis were seen.
  • These data demonstrate expression of TFFs in the endocrine pancreas, but their possible functions remain unknown.
  • [MeSH-major] Growth Hormone / metabolism. Islets of Langerhans / metabolism. Peptides / metabolism
  • [MeSH-minor] Adult. Animals. Animals, Newborn. Apoptosis / drug effects. Cell Movement / drug effects. Cell Proliferation / drug effects. Gene Expression Regulation. Humans. Insulin / secretion. Insulinoma / metabolism. Insulinoma / secretion. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / secretion. Rats. Tissue Distribution. Tumor Cells, Cultured

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  • (PMID = 16973727.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 0 / Peptides; 0 / TFF3 protein, human; 146046-78-8 / trefoil factor; 9002-72-6 / Growth Hormone
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35. Henopp T, Anlauf M, Schmitt A, Schlenger R, Zalatnai A, Couvelard A, Ruszniewski P, Schaps KP, Jonkers YM, Speel EJ, Pellegata NS, Heitz PU, Komminoth P, Perren A, Klöppel G: Glucagon cell adenomatosis: a newly recognized disease of the endocrine pancreas. J Clin Endocrinol Metab; 2009 Jan;94(1):213-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagon cell adenomatosis: a newly recognized disease of the endocrine pancreas.
  • BACKGROUND: Glucagon-producing tumors are either solitary neoplasms of the pancreas, occasionally associated with a glucagonoma syndrome, or multiple neoplasms associated with multiple endocrine neoplasia type 1 (MEN1).
  • We observed a previously undescribed multicentric glucagon-producing tumor disease that is not related to MEN1.
  • In addition, many islets were unusually large and showed glucagon cell hyperplasia.
  • There was no clinical or molecular evidence of any hereditary tumor disease, and changes in the MEN1 gene were only seen in individual tumors.
  • CONCLUSIONS: The findings are sufficiently distinctive to suggest a new neoplastic disease of the endocrine pancreas that we recommend calling glucagon cell adenomatosis.
  • [MeSH-minor] Adult. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Male. Proto-Oncogene Proteins / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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  • (PMID = 18957496.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9007-92-5 / Glucagon; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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36. Lyttle BM, Li J, Krishnamurthy M, Fellows F, Wheeler MB, Goodyer CG, Wang R: Transcription factor expression in the developing human fetal endocrine pancreas. Diabetologia; 2008 Jul;51(7):1169-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcription factor expression in the developing human fetal endocrine pancreas.
  • AIMS/HYPOTHESIS: Morphological changes that occur during pancreatic endocrine cell differentiation have been shown in rodent systems to be dependent on sequential alterations in transcription factor expression.
  • METHODS: Human fetal pancreases were examined at early (8-12 weeks of fetal age), middle (14-16 weeks) and late (19-21 weeks) stages, using immunohistological, microarray and qRT-PCR analyses.
  • Given that neurogenin 3 (NGN3) expression is critical for establishing the endocrine cell programme in the rodent pancreas, we examined its expression pattern and co-localisation in PDX-1(+), insulin(+) and glucagon(+) cells.
  • Our microarray and co-localisation analyses of transcription factors linked to NGN3 demonstrated that ISL1 transcription factor (ISL1), neurogenic differentiation 1 (NEUROD1), NK2 related transcription factor related, locus 2 (NKX2-2) and paired box gene 6 (PAX6) were upregulated during development and present in all four endocrine cell types, while NK6 related transcription factor related, locus 1 (NKX6-1) was expressed exclusively in beta cells.
  • CONCLUSIONS/INTERPRETATION: This study is an important step towards identifying key molecular factors involved in development of the human fetal endocrine pancreas.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Developmental. Pancreas / embryology. Pancreas / physiology. Transcription Factors / genetics

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  • (PMID = 18491072.001).
  • [ISSN] 0012-186X
  • [Journal-full-title] Diabetologia
  • [ISO-abbreviation] Diabetologia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers; 0 / FOXA2 protein, human; 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Hepatocyte Nuclear Factor 6; 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / NEUROG3 protein, human; 0 / Nerve Tissue Proteins; 0 / Nkx-2.2 homedomain protein; 0 / ONECUT1 protein, human; 0 / PAX4 protein, human; 0 / Paired Box Transcription Factors; 0 / Snail Family Transcription Factors; 0 / Trans-Activators; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta
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37. Rukstalis JM, Habener JF: Snail2, a mediator of epithelial-mesenchymal transitions, expressed in progenitor cells of the developing endocrine pancreas. Gene Expr Patterns; 2007 Feb;7(4):471-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Snail2, a mediator of epithelial-mesenchymal transitions, expressed in progenitor cells of the developing endocrine pancreas.
  • The mammalian pancreas develops by the expansion and morphogenesis of the epithelial cells of the foregut endoderm via the sequential activation of transcription factors that direct differentiation into the various pancreatic lineages.
  • We report the identification of the expression of the transcription factor Snail2/Slug, a known inducer of EMT and cell movement, in both the endocrine and exocrine cells of the developing mouse pancreas.
  • Snail2 is expressed in Neurogenin3-positive endocrine progenitor cells, and expression is maintained during endocrine cell differentiation where it becomes increasingly restricted to the insulin-producing beta cells and somatostatin-producing delta cells.
  • In the adult pancreas, the expression of Snail2 is maintained at low but detectable levels in all beta cells, indicating a latent role for Snail2 in the mature islet.
  • These findings of Snail2 expression during endocrine pancreas development are relevant to the recent evidence demonstrating the involvement of EMT in the expansion of human islet tissue in vitro.
  • EMT-like events appear to be involved in the development of the mammalian pancreas in vivo.

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  • (PMID = 17185046.001).
  • [ISSN] 1567-133X
  • [Journal-full-title] Gene expression patterns : GEP
  • [ISO-abbreviation] Gene Expr. Patterns
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007028; United States / NIDDK NIH HHS / DK / DK061251-03; United States / NIDDK NIH HHS / DK / DK055365-05; United States / NIDDK NIH HHS / DK / U19 DK061251-03S1; United States / NIDDK NIH HHS / DK / DK55365; United States / NIDDK NIH HHS / DK / DK061251-03S1; United States / NIDDK NIH HHS / DK / P30 DK057521; United States / NIDDK NIH HHS / DK / U19 DK061251; United States / NIDDK NIH HHS / DK / P30 DK057521-06; United States / NIDDK NIH HHS / DK / DK7028-29; United States / NIDDK NIH HHS / DK / R01 DK055365; United States / NIDDK NIH HHS / DK / DK61251; United States / NIDDK NIH HHS / DK / U19 DK061251-03; United States / NIDDK NIH HHS / DK / R01 DK055365-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cadherins; 0 / Nerve Tissue Proteins; 0 / Neurog3 protein, mouse; 0 / Transcription Factors; 0 / snail family transcription factors
  • [Other-IDs] NLM/ NIHMS28872; NLM/ PMC2698037
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38. Ballian N, Brunicardi FC: Islet vasculature as a regulator of endocrine pancreas function. World J Surg; 2007 Apr;31(4):705-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Islet vasculature as a regulator of endocrine pancreas function.
  • The islets of Langerhans consist of endocrine cells embedded in a network of specialized capillaries that regulate islet blood flow.
  • Despite evidence for a critical role of islet perfusion in endocrine pancreas function, there is information to support no fewer than three models of endocrine cell perfusion, emphasizing the lack of a universally accepted physiological theory.
  • In addition, islet perfusion determines communication between endocrine and exocrine cells and between different types of endocrine cells within islets.
  • Interest in islet microcirculation has increased after improvements in islet transplantation, a therapy for diabetes mellitus that requires revascularization of grafted islets in a new host organ.
  • Similarly, angiogenesis has been shown to be a critical step in the transformation of islet hyperplasia to neoplasia.
  • [MeSH-major] Islets of Langerhans / anatomy & histology. Islets of Langerhans / physiology

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  • (PMID = 17347899.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 102
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39. Hashimoto H, Moritani N, Terada M, Kromkhun P, Fungfuaug W, Nakada T, Yokosuka M, Saito TR: Improvement of hyperglycemia and sexual dysfunction in diabetic female rats by an artificial endocrine pancreas developed from mouse beta cells. Exp Anim; 2010;59(4):515-9
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  • [Title] Improvement of hyperglycemia and sexual dysfunction in diabetic female rats by an artificial endocrine pancreas developed from mouse beta cells.
  • We investigated the effects of a bioartificial endocrine pancreas (Bio-AEP) produced by mouse beta cells on sexual dysfunction of streptozotocin (STZ)-induced diabetic female rats.

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  • (PMID = 20660998.001).
  • [ISSN] 1881-7122
  • [Journal-full-title] Experimental animals
  • [ISO-abbreviation] Exp. Anim.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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40. Rafacho A, Quallio S, Ribeiro DL, Taboga SR, Paula FM, Boschero AC, Bosqueiro JR: The adaptive compensations in endocrine pancreas from glucocorticoid-treated rats are reversible after the interruption of treatment. Acta Physiol (Oxf); 2010 Nov;200(3):223-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The adaptive compensations in endocrine pancreas from glucocorticoid-treated rats are reversible after the interruption of treatment.
  • Islets from DEX rats secreted more insulin in response to increasing concentrations of glucose and other metabolic and non-metabolic stimuli, compared with that in the CTL group.
  • The insulin secretion for the most compounds studied returned to CTL values in DEX(10) islets.
  • Increased insulin secretion correlated well with the augmentation in β-cell proliferation and mass in DEX rats, and these morphological alterations were normalized in islets from DEX(10) rats.
  • In parallel, the increased levels of proteins involved in β-cell proliferation such as Cd2 and Cdk4 observed in DEX islets were also normalized in DEX(10) islets.
  • CONCLUSION: These data strongly support the view that almost all the morphophysiological alterations induced by dexamethasone in the endocrine pancreas are reverted after discontinuation of the treatment.
  • [MeSH-major] Dexamethasone / analogs & derivatives. Glucocorticoids / administration & dosage. Insulin / secretion. Islets of Langerhans / drug effects

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  • [Copyright] © 2010 The Authors. Journal compilation © 2010 Scandinavian Physiological Society.
  • (PMID = 20456283.001).
  • [ISSN] 1748-1716
  • [Journal-full-title] Acta physiologica (Oxford, England)
  • [ISO-abbreviation] Acta Physiol (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Cell Cycle Proteins; 0 / Glucocorticoids; 0 / Insulin; 312-93-6 / dexamethasone 21-phosphate; 7S5I7G3JQL / Dexamethasone
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41. Chen M, Rahman L, Voeller D, Kastanos E, Yang SX, Feigenbaum L, Allegra C, Kaye FJ, Steeg P, Zajac-Kaye M: Transgenic expression of human thymidylate synthase accelerates the development of hyperplasia and tumors in the endocrine pancreas. Oncogene; 2007 Jul 19;26(33):4817-24
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  • [Title] Transgenic expression of human thymidylate synthase accelerates the development of hyperplasia and tumors in the endocrine pancreas.
  • To investigate the role of deregulated TS activity in tumor development, we generated transgenic mice that express high levels of catalytically active human TS (hTS) exclusively in the pancreas and low levels of hTS in multiple other tissues.
  • Analyses of pancreatic tissue in TS transgenic mice revealed abnormalities within the endocrine pancreas, ranging from pancreatic islet hyperplasia to the detection of islet cell tumors.
  • Overexpression of hTS in murine islets provides a new model to study genetic alterations associated with the progression from normal cells to hyperplasia to islet cell tumors, and suggests that this mouse model may be useful for regulating TS activity in vivo for development of cancer prevention and new therapies.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology. Thymidylate Synthase / metabolism

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  • (PMID = 17297449.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.1.1.45 / Thymidylate Synthase
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42. Amselgruber WM, Büttner M, Schlegel T, Schweiger M, Pfaff E: The normal cellular prion protein (PrPc) is strongly expressed in bovine endocrine pancreas. Histochem Cell Biol; 2006 Apr;125(4):441-8
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  • [Title] The normal cellular prion protein (PrPc) is strongly expressed in bovine endocrine pancreas.
  • In this work we have studied whether PrP(c), a protein found predominantly in neurons, could also exist in pancreatic endocrine cells since neuroectoderm-derived cells and pancreatic islet cells share a large number of similarities.
  • Using immunostained serial sections and specific antibodies against bovine PrP(c), insulin, glucagon, somatostatin, chromogranin A and chromogranin B we found that PrP(c) is highly expressed in all endocrine cells of fetal and adult pancreatic islets with a particular strong expression in A-cells.
  • The selective expression of PrP(c) in the bovine endocrine pancreas is of particular importance regarding possible iatrogenic transmission routes and demonstrates also that bovine pancreatic islet cells could represent an interesting model to study the control of PrP-gene expression.
  • [MeSH-major] Islets of Langerhans / metabolism. PrPC Proteins / metabolism

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  • (PMID = 16208484.001).
  • [ISSN] 0948-6143
  • [Journal-full-title] Histochemistry and cell biology
  • [ISO-abbreviation] Histochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Chromogranin A; 0 / Chromogranin B; 0 / PrPC Proteins
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43. Boom A, Lybaert P, Pollet JF, Jacobs P, Jijakli H, Golstein PE, Sener A, Malaisse WJ, Beauwens R: Expression and localization of cystic fibrosis transmembrane conductance regulator in the rat endocrine pancreas. Endocrine; 2007 Oct;32(2):197-205
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  • [Title] Expression and localization of cystic fibrosis transmembrane conductance regulator in the rat endocrine pancreas.
  • In order to understand the pathophysiology of cystic fibrosis-related diabetes (CFRD), knowledge on the possible expression and cell distribution of the cystic fibrosis transmembrane conductance regulator (CFTR) protein within the endocrine pancreas is required.
  • In this report, we establish the first evidence for expression of CFTR protein in rat pancreatic islets by using independent techniques.
  • First reverse transcriptase-polymerase chain reaction (RT-PCR) amplification showed that CFTR mRNA is present in isolated islets of Langerhans.
  • [MeSH-major] Cystic Fibrosis Transmembrane Conductance Regulator / metabolism. Glucagon-Secreting Cells / metabolism. Islets of Langerhans / metabolism

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  • (PMID = 18040894.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / RNA, Messenger; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator
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44. Portela-Gomes GM, Gayen JR, Grimelius L, Stridsberg M, Mahata SK: The importance of chromogranin A in the development and function of endocrine pancreas. Regul Pept; 2008 Nov 29;151(1-3):19-25
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  • [Title] The importance of chromogranin A in the development and function of endocrine pancreas.
  • The aim of this study was to determine whether Chga null mice display changes in the morphology and function of the endocrine pancreas.
  • RESULTS: CgA epitopes were undetectable in the islets of Chga-/- animals.
  • CgB and secretogranin II epitopes were expressed in the islets of all animal groups albeit with decreased expression in Chga-/- islets.
  • Our study shows that CgA exerts a significant influence on the endocrine pancreas with importance in maintaining islet volume, cellular composition and function.
  • [MeSH-major] Chromogranin A / physiology. Islets of Langerhans / growth & development. Islets of Langerhans / physiology

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  • [ErratumIn] Regul Pept. 2009 Feb 25;153(1-3):93
  • (PMID = 18722481.001).
  • [ISSN] 0167-0115
  • [Journal-full-title] Regulatory peptides
  • [ISO-abbreviation] Regul. Pept.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranin B; 0 / Insulin; 0 / Pancreatic Hormones; 0 / Secretogranin II; 0 / chromogranin A, mouse; 0 / chromogranin B, mouse; 0 / secretogranin 2, mouse
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45. Gustavsen CR, Pillay N, Heller RS: An immunohistochemical study of the endocrine pancreas of the African ice rat, Otomys sloggetti robertsi. Acta Histochem; 2008;110(4):294-301

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An immunohistochemical study of the endocrine pancreas of the African ice rat, Otomys sloggetti robertsi.
  • The study reported here examines the endocrine pancreas of this species using immunohistochemical techniques.
  • The islets of Langerhans were scattered in the exocrine pancreas and tended to be quite small.
  • Scattered single endocrine cells (mostly immunoreactive for insulin) were found in the exocrine pancreas and were not generally associated with ducts (as marked by pan-cytokeratin labeling).
  • The normal islet architecture of insulin in the center and glucagon, somatostatin (SS) and pancreatic polypeptide (PP) in the rim was observed, but the islets tended to have 2-3 layers of glucagon immunoreactive cells.
  • Examining for rarer endocrine cell types, we found that cocaine amphetamine regulated transcript (CART) immunoreactive cells were co-localized with SS; and peptide YY (PYY) immunoreactive cells could be found that were singly immunoreactive or co-localized with either PP or glucagon.
  • The Nkx family of transcription factors (Nkx6.1 and 2.2) and PDX-1 were all detected in the pancreas in a similar manner to that seen in mouse and rat.
  • In conclusion, the endocrine pancreas of the African ice rat is quite similar to that of other studied rodents, but these animals have more glucagon and SS cells than rat (Rattus) or mouse (Mus) species.
  • [MeSH-major] Islets of Langerhans / metabolism. Murinae / metabolism

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  • (PMID = 18406449.001).
  • [ISSN] 0065-1281
  • [Journal-full-title] Acta histochemica
  • [ISO-abbreviation] Acta Histochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hormones; 0 / Transcription Factors
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46. Okabayashi T, Maeda H, Sun ZL, Montgomery RA, Nishimori I, Hanazaki K: Perioperative insulin therapy using a closed-loop artificial endocrine pancreas after hepatic resection. World J Gastroenterol; 2009 Sep 07;15(33):4116-21
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  • [Title] Perioperative insulin therapy using a closed-loop artificial endocrine pancreas after hepatic resection.
  • Here, we review the benefits and requirements of perioperative intensive insulin therapy using a closed-loop artificial endocrine pancreas system in hepatectomized patients.

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  • (PMID = 19725143.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 35
  • [Other-IDs] NLM/ PMC2738805
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47. Souza F, Freeby M, Hultman K, Simpson N, Herron A, Witkowsky P, Liu E, Maffei A, Harris PE: Current progress in non-invasive imaging of beta cell mass of the endocrine pancreas. Curr Med Chem; 2006;13(23):2761-73
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  • [Title] Current progress in non-invasive imaging of beta cell mass of the endocrine pancreas.
  • Studies in prevention and treatment have been hampered by the single end-point of diagnosis of diabetes and hyperglycemia.
  • Many of the methods are limited by the inability to translate to the clinical setting, poor discrimination between the exocrine and endocrine pancreas, or a poor measurement of beta-cell mass.

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  • (PMID = 17073627.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / 5 P30 DK063608-02; United States / NINDS NIH HHS / NS / 2R01 NS15655; United States / Intramural NIH HHS / / ; United States / NIDDK NIH HHS / DK / R01 DK077493; United States / NIDDK NIH HHS / DK / R01 DK063567; United States / NIDDK NIH HHS / DK / 2 R01 DK63567-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 113
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48. Tano K, Oyabu A, Tashiro Y, Kamada N, Narita N, Nasu F, Narita M: Manserin, a secretogranin II-derived peptide, distributes in the rat endocrine pancreas colocalized with islet-cell specific manner. Histochem Cell Biol; 2010 Jul;134(1):53-7

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  • [Title] Manserin, a secretogranin II-derived peptide, distributes in the rat endocrine pancreas colocalized with islet-cell specific manner.
  • Although the physiological roles of manserin have not been elucidated to date, manserin has been shown to distribute in not only the brain but also the endocrine system such as the pituitary and adrenal glands, suggesting its role in the endocrine system.
  • The present study aimed to explore the occurrence and distribution of manserin in the rat pancreas using an immunohistochemical technique with a polyclonal antibody against rat manserin.
  • Immunoreactivity for manserin was readily detected in almost whole islets of Langerhans whereas not at all in the exocrine pancreas.
  • These results indicate that manserin, occurring in the endocrine pancreas, may have a potential role in the endocrine system.
  • [MeSH-major] Islets of Langerhans / metabolism. Neuropeptides / metabolism. Peptide Fragments / metabolism

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  • (PMID = 20495819.001).
  • [ISSN] 1432-119X
  • [Journal-full-title] Histochemistry and cell biology
  • [ISO-abbreviation] Histochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Neuropeptides; 0 / Peptide Fragments; 0 / manserin, rat
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49. Collombat P, Hecksher-Sørensen J, Broccoli V, Krull J, Ponte I, Mundiger T, Smith J, Gruss P, Serup P, Mansouri A: The simultaneous loss of Arx and Pax4 genes promotes a somatostatin-producing cell fate specification at the expense of the alpha- and beta-cell lineages in the mouse endocrine pancreas. Development; 2005 Jul;132(13):2969-80
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  • [Title] The simultaneous loss of Arx and Pax4 genes promotes a somatostatin-producing cell fate specification at the expense of the alpha- and beta-cell lineages in the mouse endocrine pancreas.
  • The specification of the different mouse pancreatic endocrine subtypes is determined by the concerted activities of transcription factors.
  • However, the molecular mechanisms regulating endocrine fate allocation remain unclear.
  • In the present study, we uncover the molecular consequences of the simultaneous depletion of Arx and Pax4 activity during pancreas development.
  • Specifically, in the combined absence of Arx and Pax4, an early-onset loss of mature alpha- and beta-cells occurs in the endocrine pancreas, concomitantly with a virtually exclusive generation of somatostatin-producing cells.
  • Finally, our data provide evidence that both Arx and Pax4 act as transcriptional repressors that control the expression level of one another, thereby mediating proper endocrine fate allocation.
  • [MeSH-major] Cell Differentiation / physiology. Homeodomain Proteins / genetics. Islets of Langerhans / cytology. Islets of Langerhans / embryology. Somatostatin / biosynthesis. Transcription Factors / genetics

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  • (PMID = 15930104.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] eng
  • [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.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ARX protein, mouse; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Paired Box Transcription Factors; 0 / Pax4 protein, mouse; 0 / Transcription Factors; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon
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50. Li Z, Wen C, Peng J, Korzh V, Gong Z: Generation of living color transgenic zebrafish to trace somatostatin-expressing cells and endocrine pancreas organization. Differentiation; 2009 Feb;77(2):128-34
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  • [Title] Generation of living color transgenic zebrafish to trace somatostatin-expressing cells and endocrine pancreas organization.
  • During embryonic development, expression of GFP/RFP in the endocrine pancreas of transgenic embryos was initiated at approximately 20 hpf and the number of GFP/RFP positive cells in the pancreas increased in subsequent stages; thus, our newly generated Tg(sst2:gfp) and Tg(sst2:rfp) lines faithfully recapitulated sst2 expression in endocrine pancreatic cells and provided a useful tool in analyzing the development of Sst2-producing delta-cells in the pancreas.
  • By crossing these new transgenic lines with previously available transgenic lines targeted in insulin (Ins)-producing beta-cells, Tg(ins:gfp) and Tg(ins:rfp), in combination with immunodetection of glucagon (Gcg)-producing alpha-cells and pancreatic polypeptide (PP)-producing PP-cells, the organization and composition of endocrine islets were investigated in both embryonic and adult pancreas.
  • We found that there was always a big cluster of endocrine cells (principal islet) in the anterior-dorsal pancreas, followed by numerous smaller clusters (variable in size) of endocrine cells (secondary islets) along the anterior-posterior axis of the pancreas.
  • All four types of endocrine cells were found in the principal islet, but secondary islets may or may not contain PP-cells.
  • In addition, there were also discrete endocrine cells throughout the pancreas.
  • In all co-localization experiments, we did not find any endocrine cells positive for more than one hormone markers, suggesting that these endocrine cells produce only a single hormone.
  • In both principal and secondary islets, we found that beta-cells were generally located in the center and non-beta cells in the periphery; reminiscent of the "mantel-core" organization of islets of Langerhans in mammals where beta-cells form the core and non-beta-cells the mantel.
  • In zebrafish primary islet, beta-cells constitute most of the mass (approximately 50%), followed by delta-cells and alpha-cells (20-25% each), and PP-cells (1-2%); this is also similar to the composition of mammalian islets.

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  • (PMID = 19281772.001).
  • [ISSN] 1432-0436
  • [Journal-full-title] Differentiation; research in biological diversity
  • [ISO-abbreviation] Differentiation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Luminescent Proteins; 51110-01-1 / Somatostatin
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51. Rafacho A, Giozzet VA, Boschero AC, Bosqueiro JR: Functional alterations in endocrine pancreas of rats with different degrees of dexamethasone-induced insulin resistance. Pancreas; 2008 Apr;36(3):284-93
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  • [Title] Functional alterations in endocrine pancreas of rats with different degrees of dexamethasone-induced insulin resistance.
  • At the end of the treatment, only DEX 1.0 rats showed significant increase of postabsorptive blood glucose and serum triglycerides, and nonesterified fatty acids levels.
  • Incubation of pancreatic islets in increasing glucose concentrations (2.8-22 mM) led to an augmented insulin secretion in all DEX-treated rats.
  • CONCLUSIONS: We demonstrate that in DEX 0.5 and, especially in DEX 0.1 groups, but not in DEX 1.0, the adaptations that occurred in the endocrine pancreas are able to counteract metabolic disorders (glucose intolerance and dyslipidemia).
  • [MeSH-major] Dexamethasone / toxicity. Glucocorticoids / toxicity. Insulin Resistance / physiology. Islets of Langerhans / drug effects. Islets of Langerhans / physiopathology

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  • (PMID = 18362843.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Fatty Acids, Nonesterified; 0 / Glucocorticoids; 0 / Insulin; 0 / Triglycerides; 7S5I7G3JQL / Dexamethasone; IY9XDZ35W2 / Glucose
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52. Anlauf M, Schlenger R, Perren A, Bauersfeld J, Koch CA, Dralle H, Raffel A, Knoefel WT, Weihe E, Ruszniewski P, Couvelard A, Komminoth P, Heitz PU, Klöppel G: Microadenomatosis of the endocrine pancreas in patients with and without the multiple endocrine neoplasia type 1 syndrome. Am J Surg Pathol; 2006 May;30(5):560-74
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  • [Title] Microadenomatosis of the endocrine pancreas in patients with and without the multiple endocrine neoplasia type 1 syndrome.
  • It has been suggested that microadenomatosis of the endocrine pancreas is a hallmark of the multiple endocrine neoplasia type 1 syndrome (MEN1).
  • In microadenomatosis patients with and without the MEN1 syndrome, a subset of morphologically normal-appearing islets showed increased endocrine cell proliferation.
  • In conclusion, endocrine multihormonal microadenomatosis of the pancreas is a feature of MEN1.
  • [MeSH-major] Adenoma, Islet Cell / complications. Adenoma, Islet Cell / pathology. Multiple Endocrine Neoplasia Type 1 / complications. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology


53. Rossi J, Santamäki P, Airaksinen MS, Herzig KH: Parasympathetic innervation and function of endocrine pancreas requires the glial cell line-derived factor family receptor alpha2 (GFRalpha2). Diabetes; 2005 May;54(5):1324-30
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  • [Title] Parasympathetic innervation and function of endocrine pancreas requires the glial cell line-derived factor family receptor alpha2 (GFRalpha2).
  • Vagal parasympathetic input to the islets of Langerhans is a regulator of islet hormone secretion, but factors promoting parasympathetic islet innervation are unknown.
  • Here, we show that the parasympathetic nerve fibers and glial cells within and around the islets express GFRalpha2 and that islet parasympathetic innervation in GFRalpha2 knockout (KO) mice is reduced profoundly.
  • The GFRalpha2-KO mouse represents a useful model to study the role of parasympathetic innervation of the endocrine pancreas in glucose homeostasis.
  • [MeSH-major] Islets of Langerhans / physiology. Neuroglia / physiology. Parasympathetic Nervous System / physiology. Proto-Oncogene Proteins / physiology. Receptor Protein-Tyrosine Kinases / physiology

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  • (PMID = 15855316.001).
  • [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 / Blood Glucose; 0 / Gfra2 protein, mouse; 0 / Glial Cell Line-Derived Neurotrophic Factor Receptors; 0 / Proto-Oncogene Proteins; 59763-91-6 / Pancreatic Polypeptide; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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54. Agudo J, Ayuso E, Jimenez V, Salavert A, Casellas A, Tafuro S, Haurigot V, Ruberte J, Segovia JC, Bueren J, Bosch F: IGF-I mediates regeneration of endocrine pancreas by increasing beta cell replication through cell cycle protein modulation in mice. Diabetologia; 2008 Oct;51(10):1862-72
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  • [Title] IGF-I mediates regeneration of endocrine pancreas by increasing beta cell replication through cell cycle protein modulation in mice.
  • Igf1 expression in beta cells of transgenic mice regenerates the endocrine pancreas during type 1 diabetes.
  • In contrast, higher levels of cyclin-dependent kinase inhibitor 1A (p21) were detected in islets from non-STZ-treated transgenic mice.
  • Therefore, our study suggests that local production of IGF-I may be a safe approach to regenerate endocrine pancreas to reverse diabetes.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Insulin-Like Growth Factor I / metabolism. Insulin-Secreting Cells / metabolism. Islets of Langerhans / metabolism

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  • (PMID = 18663428.001).
  • [ISSN] 0012-186X
  • [Journal-full-title] Diabetologia
  • [ISO-abbreviation] Diabetologia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Cell Cycle Proteins; 147336-22-9 / Green Fluorescent Proteins; 5W494URQ81 / Streptozocin; 67763-96-6 / Insulin-Like Growth Factor I
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55. Louagie E, Taylor NA, Flamez D, Roebroek AJ, Bright NA, Meulemans S, Quintens R, Herrera PL, Schuit F, Van de Ven WJ, Creemers JW: Role of furin in granular acidification in the endocrine pancreas: identification of the V-ATPase subunit Ac45 as a candidate substrate. Proc Natl Acad Sci U S A; 2008 Aug 26;105(34):12319-24
SciCrunch. OMIM: Data: Gene Annotation .

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  • [Title] Role of furin in granular acidification in the endocrine pancreas: identification of the V-ATPase subunit Ac45 as a candidate substrate.
  • The effect of genetic ablation of fur was studied in the endocrine pancreas to define its physiological function in the regulated secretory pathway.
  • Ac45 is highly expressed in islets of Langerhans and furin was able to cleave Ac45 ex vivo.
  • [MeSH-major] Cytoplasmic Granules / metabolism. Furin / physiology. Islets of Langerhans / metabolism. Vacuolar Proton-Translocating ATPases / metabolism
  • [MeSH-minor] Animals. Binding Sites. Cell Line, Tumor. Hydrogen-Ion Concentration. Insulin / secretion. Insulinoma. Mice. Mice, Knockout. Substrate Specificity

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  • (PMID = 18713856.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Atp6ap1 protein, mouse; 0 / Insulin; EC 3.4.21.75 / Furin; EC 3.6.1.- / Vacuolar Proton-Translocating ATPases
  • [Other-IDs] NLM/ PMC2527909
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56. Capurso G, Crnogorac-Jurcevic T, Milione M, Panzuto F, Campanini N, Dowen SE, Di Florio A, Sette C, Bordi C, Lemoine NR, Delle Fave G: Peanut-like 1 (septin 5) gene expression in normal and neoplastic human endocrine pancreas. Neuroendocrinology; 2005;81(5):311-21
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  • [Title] Peanut-like 1 (septin 5) gene expression in normal and neoplastic human endocrine pancreas.
  • As the secretory apparatus of pancreatic islet cells closely resembles that of neurons, we decided to study the expression of PNUTL1 in the human endocrine pancreas, both in normal islets and in pancreatic endocrine tumors (PETs).
  • Normal pancreatic tissue, purified islets, 11 PETs and two cell lines were used to evaluate the presence of PNUTL1 by RT-PCR and Western blot.
  • The expression of the PNUTL1 protein was also evaluated by immunohistochemistry on normal pancreas, additional 26 PETs, eight pancreatic adenocarcinomas, one mixed endocrine-exocrine pancreatic neoplasm, a specimen of solid papillary pseudomucinous tumor, an adult islet cell hyperplasia and a case of neonatal nesidioblastosis.
  • In addition, a tissue array (LandMark High Density Cancer Tissue MicroArray) comprising 280 various tumor and matched normal specimens was utilized.
  • In the normal pancreas PNUTL1 expression is almost exclusively confined to the islet cells, weak expression was occasionally seen in some acinar cells, while immunoreactivity was completely absent in the ductal epithelia.
  • Our findings describe for the first time the high expression levels of PNUTL1 in human pancreatic endocrine cells that suggests a similar role of this protein in islet cells to that demonstrated in neuronal tissues, and warrants further functional studies of this protein.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Gene Expression / physiology. Gene Expression Regulation, Neoplastic / physiology. Islets of Langerhans / metabolism. Pancreatic Neoplasms / metabolism

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16179808.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / RNA, Messenger; EC 3.6.1.- / SEPT5 protein, human; EC 3.6.1.- / Septins
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57. Moulin P, Guiot Y, Jonas JC, Rahier J, Devuyst O, Henquin JC: Identification and subcellular localization of the Na+/H+ exchanger and a novel related protein in the endocrine pancreas and adrenal medulla. J Mol Endocrinol; 2007 Mar;38(3):409-22
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  • [Title] Identification and subcellular localization of the Na+/H+ exchanger and a novel related protein in the endocrine pancreas and adrenal medulla.
  • Na+/H+ exchangers (NHE) constitute a family of membrane antiporters that contribute to the regulation of cellular pH and volume in many tissues, including pancreatic islets.
  • We investigated the molecular identity of NHE in rodent and human endocrine pancreas, and determined its cellular and subcellular localization.
  • NHE1 was the most abundantly expressed isoform in rat islets, and was also expressed in mouse and human islets.
  • By western blot, an antiserum raised against the C-terminus end of NHE1 confirmed the presence of a ~100 kDa protein corresponding to NHE1 in islets and unexpectedly unveiled the existence of a ~65 kDa cross-reactive NHE1-related protein.
  • By immunohistochemistry, the antiserum labelled the membranes of pancreatic acini and ducts, but also diffusely stained the cytoplasm of insulin, glucagon and somatostatin cells as well as endocrine cells of the adrenal medulla.
  • Islets of Slc9A1(swe/swe) mice, which lack full NHE1 protein, were found to express an mRNA corresponding to the 3' end of NHE1 as well as the ~65 kDa protein.
  • We conclude that both the full-length and the shorter-splice variant of NHE1 are expressed in all cell types of the endocrine pancreas and in the adrenal medulla of rodents and humans.
  • [MeSH-major] Adrenal Medulla / metabolism. Pancreas / metabolism. Sodium-Hydrogen Antiporter / metabolism. Subcellular Fractions / metabolism

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  • (PMID = 17339404.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Sodium-Hydrogen Antiporter
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58. Ichimori S, Nishida K, Shimoda S, Sekigami T, Matsuo Y, Ichinose K, Shichiri M, Sakakida M, Araki E: Development of a highly responsive needle-type glucose sensor using polyimide for a wearable artificial endocrine pancreas. J Artif Organs; 2006;9(2):105-13
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  • [Title] Development of a highly responsive needle-type glucose sensor using polyimide for a wearable artificial endocrine pancreas.
  • To produce a long-life, stable, miniature glucose sensor for a wearable artificial endocrine pancreas (WAEP), we developed a novel microneedle-type glucose sensor using polyimide, designated the PI sensor (outer diameter, 0.3 mm; length, 16 mm), and investigated its characteristics in vitro and in vivo.
  • [MeSH-major] Blood Glucose / analysis. Imides. Pancreas, Artificial

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  • (PMID = 16807813.001).
  • [ISSN] 1434-7229
  • [Journal-full-title] Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs
  • [ISO-abbreviation] J Artif Organs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Imides; IY9XDZ35W2 / Glucose
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59. Dromain C, Baudin E: [Endocrine pancreas]. J Radiol; 2005 Jun;86(6 Pt 2):797-804; quiz 805
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  • [Title] [Endocrine pancreas].
  • [Transliterated title] Pancréas endocrine.
  • Pancreatic endocrine tumors (PET) are characterised by their hormone synthesis capability and can be associated with an hereditary syndrome-related cancer.
  • The challenge for imaging is to localize the tumor.
  • Non-functioning PET frequently are large and malignant with metastases at the time of diagnosis.
  • [MeSH-major] Diagnostic Imaging. Islets of Langerhans / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / diagnosis. Endosonography. Humans. Magnetic Resonance Imaging. Positron-Emission Tomography. Somatostatin. Tomography, X-Ray Computed

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  • (PMID = 16142073.001).
  • [ISSN] 0221-0363
  • [Journal-full-title] Journal de radiologie
  • [ISO-abbreviation] J Radiol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 51110-01-1 / Somatostatin
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60. Anlauf M, Sipos B, Klöppel G: [Tumors of the endocrine pancreas]. Pathologe; 2005 Feb;26(1):46-51
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  • [Title] [Tumors of the endocrine pancreas].
  • [Transliterated title] Tumoren des endokrinen Pankreas.
  • The neuroendocrine tumors of the pancreas are rare, but belong to the most common endocrine neoplasms of the abdomen.
  • Using morphological, immunohistochemical and biological criteria, the classification distinguishes between well differentiated tumors with benign or uncertain behavior, well differentiated (low grade malignant) carcinomas and poorly differentiated (high grade malignant) carcinomas.
  • [MeSH-major] Carcinoma, Neuroendocrine / pathology. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 15586284.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
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61. Peschke E: Melatonin, endocrine pancreas and diabetes. J Pineal Res; 2008 Jan;44(1):26-40
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  • [Title] Melatonin, endocrine pancreas and diabetes.
  • A third system, the IP(3)-pathway, is mediated by G(q)-proteins, phospholipase C and IP(3), which mobilize Ca(2+) from intracellular stores, with a resultant increase in insulin. (iii) Insulin secretion in vivo, as well as from isolated islets, exhibits a circadian rhythm.
  • This rhythm, which is apparently generated within the islets, is influenced by melatonin, which induces a phase shift in insulin secretion. (iv) Observation of the circadian expression of clock genes in the pancreas could possibly be an indication of the generation of circadian rhythms in the pancreatic islets themselves. (v) Melatonin influences diabetes and associated metabolic disturbances.
  • [MeSH-major] Biological Clocks / genetics. Diabetes Mellitus / metabolism. Glucose / metabolism. Insulin / secretion. Islets of Langerhans / physiology. Melatonin / physiology

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  • (PMID = 18078445.001).
  • [ISSN] 0742-3098
  • [Journal-full-title] Journal of pineal research
  • [ISO-abbreviation] J. Pineal Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Free Radicals; 0 / Insulin; 0 / Receptors, Melatonin; 5W494URQ81 / Streptozocin; 6SW5YHA5NG / Alloxan; IY9XDZ35W2 / Glucose; JL5DK93RCL / Melatonin
  • [Number-of-references] 214
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62. Dhawan S, Georgia S, Bhushan A: Formation and regeneration of the endocrine pancreas. Curr Opin Cell Biol; 2007 Dec;19(6):634-45
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  • [Title] Formation and regeneration of the endocrine pancreas.
  • The elaboration of the pancreas from epithelial buds to the intricate organ requires complex patterning information that controls fundamental cellular processes such as differentiation and proliferation of pancreatic progenitor cells.
  • During pancreatic organogenesis, endocrine cells are generated from a population of pancreatic progenitor cells.
  • The endocrine cells that differentiate from progenitor cells are postmitotic, and direct lineage tracing analyses indicate that a population of progenitor cells persists throughout embryogenesis to allow the differentiation of new endocrine cells.
  • At the end of embryogenesis an early postnatal period is characterized by high rates of beta cell proliferation leading to massive increases in beta cell mass.

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  • (PMID = 18061427.001).
  • [ISSN] 0955-0674
  • [Journal-full-title] Current opinion in cell biology
  • [ISO-abbreviation] Curr. Opin. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK068763-02; United States / NIDDK NIH HHS / DK / R01 DK068763; United States / NIDDK NIH HHS / DK / R01 DK-068763; United States / NIDDK NIH HHS / DK / R01 DK068763-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 110
  • [Other-IDs] NLM/ NIHMS36362; NLM/ PMC2695413
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63. Hammerman MR: Growing new endocrine pancreas in situ. Clin Exp Nephrol; 2006 Mar;10(1):1-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growing new endocrine pancreas in situ.
  • Embryonic pancreatic primordia transplanted into diabetic animal hosts undergo selective endocrine differentiation in situ and normalize glucose tolerance.
  • [MeSH-major] Organogenesis. Pancreas / embryology. Pancreas, Artificial. Tissue Engineering / methods

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  • (PMID = 16544171.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 24
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64. Gradwohl G: Development of the endocrine pancreas. Diabetes Metab; 2006 Dec;32(5 Pt 2):532-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of the endocrine pancreas.
  • This short review presents the recent breakthroughts in our understanding of the important steps controlling pancreas morphogenesis and differentiation, and on the transcription factors regulating pancreas organogenesis and islet cell differentiation and involved in the specification of the beta and alpha cell lineages.
  • [MeSH-major] Islets of Langerhans / growth & development

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  • (PMID = 17130813.001).
  • [ISSN] 1262-3636
  • [Journal-full-title] Diabetes & metabolism
  • [ISO-abbreviation] Diabetes Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Transcription Factors
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65. Mellitzer G, Bonné S, Luco RF, Van De Casteele M, Lenne-Samuel N, Collombat P, Mansouri A, Lee J, Lan M, Pipeleers D, Nielsen FC, Ferrer J, Gradwohl G, Heimberg H: IA1 is NGN3-dependent and essential for differentiation of the endocrine pancreas. EMBO J; 2006 Mar 22;25(6):1344-52
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IA1 is NGN3-dependent and essential for differentiation of the endocrine pancreas.
  • Neurogenin 3 (Ngn3) is key for endocrine cell specification in the embryonic pancreas and induction of a neuroendocrine cell differentiation program by misexpression in adult pancreatic duct cells.
  • During embryonic development of the pancreas, IA1 and Ngn3 exhibit nearly identical spatio-temporal expression patterns.
  • However, embryos lacking Ngn3 fail to express IA1 in the pancreas.
  • IA1 is an effector of Ngn3 function as inhibition of IA1 expression in embryonic pancreas decreases the formation of insulin- and glucagon-positive cells by 40%, while its ectopic expression amplifies neuroendocrine cell differentiation by Ngn3 in adult duct cells.
  • IA1 is therefore a novel Ngn3-regulated factor required for normal differentiation of pancreatic endocrine cells.

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 16511571.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / U19 DK072495; United States / NIDDK NIH HHS / DK / DK072495-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ARX protein, mouse; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Nerve Tissue Proteins; 0 / Neurod1 protein, mouse; 0 / Neurog3 protein, mouse; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / Pax4 protein, mouse; 0 / Repressor Proteins; 0 / Transcription Factors; 147955-03-1 / INSM1 protein, human; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ PMC1422151
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66. Hammerman MR: Organogenesis of kidney and endocrine pancreas: the window opens. Organogenesis; 2007 Oct;3(2):59-66
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Organogenesis of kidney and endocrine pancreas: the window opens.
  • Pancreatic primordia can be transplanted across the same barriers undergo growth, and differentiation of endocrine components only and secrete insulin in a physiological manner following mesenteric placement.

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  • (PMID = 19279701.001).
  • [ISSN] 1547-6278
  • [Journal-full-title] Organogenesis
  • [ISO-abbreviation] Organogenesis
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK079333
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2649619
  • [Keywords] NOTNLM ; chronic kidney disease / diabetes mellitus / non-human primates / transplantation / xenotransplantation / β-cell
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67. Bermúdez-Silva FJ, Suárez J, Baixeras E, Cobo N, Bautista D, Cuesta-Muñoz AL, Fuentes E, Juan-Pico P, Castro MJ, Milman G, Mechoulam R, Nadal A, Rodríguez de Fonseca F: Presence of functional cannabinoid receptors in human endocrine pancreas. Diabetologia; 2008 Mar;51(3):476-87
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Presence of functional cannabinoid receptors in human endocrine pancreas.
  • AIMS/HYPOTHESIS: We examined the presence of functional cannabinoid receptors 1 and 2 (CB1, CB2) in isolated human islets, phenotyped the cells producing cannabinoid receptors and analysed the actions of selective cannabinoid receptor agonists on insulin, glucagon and somatostatin secretion in vitro.
  • Static secretion experiments were used to examine the effects of activating CB1 or CB2 on insulin, glucagon and somatostatin secretion and to measure changes in 2-arachidonoylglycerol (2-AG) levels within islets.
  • Analyses were performed in isolated human islets and in paraffin-embedded sections of human pancreas.
  • RESULTS: Human islets of Langerhans expressed CB1 and CB2 (also known as CNR1 and CNR2) mRNA and CB1 and CB2 proteins, and also the machinery involved in synthesis and degradation of 2-AG (the most abundant endocannabinoid, levels of which were modulated by glucose).
  • CONCLUSIONS/INTERPRETATION: Together, these results suggest a role for endogenous endocannabinoid signalling in regulation of endocrine secretion in the human pancreas.
  • [MeSH-major] Islets of Langerhans / physiology. Receptor, Cannabinoid, CB1 / physiology. Receptor, Cannabinoid, CB2 / physiology

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  • (PMID = 18092149.001).
  • [ISSN] 0012-186X
  • [Journal-full-title] Diabetologia
  • [ISO-abbreviation] Diabetologia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cannabinoids; 0 / RNA, Messenger; 0 / Receptor, Cannabinoid, CB1; 0 / Receptor, Cannabinoid, CB2; 9007-92-5 / Glucagon
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68. Hettiarachchi KD, Zimmet PZ, Myers MA: The effects of repeated exposure to sub-toxic doses of plecomacrolide antibiotics on the endocrine pancreas. Food Chem Toxicol; 2006 Dec;44(12):1966-77
Hazardous Substances Data Bank. STREPTOZOTOCIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effects of repeated exposure to sub-toxic doses of plecomacrolide antibiotics on the endocrine pancreas.
  • The plecomacrolide vacuolar ATPase inhibitors bafilomycin and concanamycin contaminate tuberous vegetables and damage pancreatic islets in mice.
  • We conclude that repeated exposure to small quantities of vacuolar proton-translocating ATPase inhibitory plecomacrolides reduces islet size and can lead to glucose intolerance, possibly due to impaired maintenance of pancreatic islets.
  • [MeSH-major] Anti-Bacterial Agents / toxicity. Enzyme Inhibitors / toxicity. Islets of Langerhans / drug effects. Macrolides / toxicity. Proton-Translocating ATPases / antagonists & inhibitors

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  • (PMID = 16905235.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Blood Glucose; 0 / Enzyme Inhibitors; 0 / Insulin; 0 / Macrolides; 5W494URQ81 / Streptozocin; 80890-47-7 / concanamycin A; 88899-55-2 / bafilomycin A1; EC 3.6.3.14 / Proton-Translocating ATPases
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69. Villasenor A, Wang ZV, Rivera LB, Ocal O, Asterholm IW, Scherer PE, Brekken RA, Cleaver O, Wilkie TM: Rgs16 and Rgs8 in embryonic endocrine pancreas and mouse models of diabetes. Dis Model Mech; 2010 Sep-Oct;3(9-10):567-80
Xenbase. Xenbase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rgs16 and Rgs8 in embryonic endocrine pancreas and mouse models of diabetes.
  • Novel approaches are needed to discover new therapeutics and to understand the contributions of endocrine progenitors and beta-cell regeneration during islet expansion.
  • Here, we show that the regulators of G protein signaling Rgs16 and Rgs8 are expressed in pancreatic progenitor and endocrine cells during development, then extinguished in adults, but reactivated in models of both type 1 and type 2 diabetes.
  • [MeSH-major] Diabetes Mellitus, Type 1 / embryology. Diabetes Mellitus, Type 1 / pathology. Islets of Langerhans / embryology. Islets of Langerhans / pathology. RGS Proteins / metabolism

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  • Guide to Pharmacology. gene/protein/disease-specific - regulator of G-protein signaling 16 - data and references .
  • Guide to Pharmacology. gene/protein/disease-specific - regulator of G-protein signaling 8 - data and references .
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  • (PMID = 20616094.001).
  • [ISSN] 1754-8411
  • [Journal-full-title] Disease models & mechanisms
  • [ISO-abbreviation] Dis Model Mech
  • [Language] eng
  • [Grant] United States / PHS HHS / / R0161395; United States / NIMH NIH HHS / MH / P50MH066172; United States / NCI NIH HHS / CA / R01CA118240; United States / NIDDK NIH HHS / DK / DK079862; United States / NIDDK NIH HHS / DK / R01 DK079862; United States / NIMH NIH HHS / MH / P50 MH066172; United States / NIGMS NIH HHS / GM / R01 GM061395; United States / NCI NIH HHS / CA / R01 CA118240
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptides; 0 / RGS Proteins; 0 / RGS16 protein; 0 / RGS8 protein, mouse; 0 / Recombinant Fusion Proteins; 0 / Venoms; 147336-22-9 / Green Fluorescent Proteins; 9P1872D4OL / exenatide
  • [Other-IDs] NLM/ PMC2931535
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70. Gangaram-Panday ST, Faas MM, de Vos P: Towards stem-cell therapy in the endocrine pancreas. Trends Mol Med; 2007 Apr;13(4):164-73
MedlinePlus Health Information. consumer health - Islet Cell Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Towards stem-cell therapy in the endocrine pancreas.
  • One is the application of stem cells for replacement of nonfunctional islet cells in the native endogenous pancreas; another one is the use of stem cells as an inexhaustible source for islet-cell transplantation.
  • The applicability for the treatment of dysfunction of beta cells in the pancreas has been demonstrated for all three cell types, but more-detailed understanding of the sequence of events during differentiation is required to produce fully functional insulin-producing cells.
  • [MeSH-major] Islets of Langerhans Transplantation / trends
  • [MeSH-minor] Animals. Diabetes Mellitus / surgery. Embryonic Stem Cells / transplantation. Hematopoietic Stem Cell Transplantation. Humans. Islets of Langerhans / embryology. Islets of Langerhans / growth & development. Islets of Langerhans / metabolism. Models, Biological. Stem Cell Transplantation. Transcription Factors / metabolism

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  • (PMID = 17307397.001).
  • [ISSN] 1471-4914
  • [Journal-full-title] Trends in molecular medicine
  • [ISO-abbreviation] Trends Mol Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transcription Factors
  • [Number-of-references] 79
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71. Palumbo P, De Gaetano A: An islet population model of the endocrine pancreas. J Math Biol; 2010 Aug;61(2):171-205

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An islet population model of the endocrine pancreas.
  • Without detailing the chain of biochemical events giving rise to the delivery of insulin packets, the effect of the islets' bursting response to varying glucose concentration is described by a simple second order nonlinear model, of the same functional form for all islets, but with a random distribution of parameter values over the one million islets considered.
  • [MeSH-major] Islets of Langerhans / cytology. Islets of Langerhans / metabolism. Models, Biological

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  • (PMID = 19756607.001).
  • [ISSN] 1432-1416
  • [Journal-full-title] Journal of mathematical biology
  • [ISO-abbreviation] J Math Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin
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72. Huang YH, Sun MJ, Jiang M, Fu BY: Immunohistochemical localization of glucagon and pancreatic polypeptide on rat endocrine pancreas: coexistence in rat islet cells. Eur J Histochem; 2009 Apr-Jun;53(2):81-5
Hazardous Substances Data Bank. GLUCAGON .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical localization of glucagon and pancreatic polypeptide on rat endocrine pancreas: coexistence in rat islet cells.
  • We used immunofluorescence double staining method to investigate the cellular localization of glucagon and pancreatic polypeptide (PP) in rat pancreatic islets.
  • The results showed that both A-cells (glucagon-secreting cells) and PP-cells (PP-secreting cells) were located in the periphery of the islets.
  • Most of A-cells were located in the splenic lobe but a few of them were in the duodenal lobe of the pancreas.
  • In contrast, the majority of PP-cells were found in the duodenal lobe and a few of them were in the splenic lobe of the pancreas.
  • [MeSH-major] Glucagon / metabolism. Glucagon-Secreting Cells / metabolism. Islets of Langerhans / cytology. Islets of Langerhans / metabolism. Pancreatic Polypeptide / metabolism. Pancreatic Polypeptide-Secreting Cells / metabolism

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  • (PMID = 19683981.001).
  • [ISSN] 1121-760X
  • [Journal-full-title] European journal of histochemistry : EJH
  • [ISO-abbreviation] Eur J Histochem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 59763-91-6 / Pancreatic Polypeptide; 9007-92-5 / Glucagon
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73. Stetsyuk V, Peers B, Mavropoulos A, Verbruggen V, Thisse B, Thisse C, Motte P, Duvillié B, Scharfmann R: Calsenilin is required for endocrine pancreas development in zebrafish. Dev Dyn; 2007 Jun;236(6):1517-25
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calsenilin is required for endocrine pancreas development in zebrafish.
  • We detected calsenilin transcripts in the pancreas from 21 somites to 39 hours postfertilization stages.
  • Using double in situ hybridization, we found that the calsenilin gene was expressed in pancreatic endocrine cells.
  • Loss-of-function experiments with anti-calsenilin morpholinos demonstrated that injected morphants have a significant decrease in the number of pancreatic endocrine cells.
  • Taken together, our results show that zebrafish calsenilin is involved in endocrine cell differentiation and morphogenesis within the pancreas.
  • [MeSH-major] Endocrine System / embryology. Endocrine System / metabolism. Kv Channel-Interacting Proteins / metabolism. Pancreas / embryology. Pancreas / metabolism. Zebrafish / embryology. Zebrafish / metabolism

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • [Copyright] Copyright 2007 Wiley-Liss, Inc.
  • (PMID = 17450605.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Kv Channel-Interacting Proteins; 0 / Pancreatic Hormones; 0 / Receptors, Notch; 5688UTC01R / Tretinoin
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74. Ait-Lounis A, Baas D, Barras E, Benadiba C, Charollais A, Nlend Nlend R, Liègeois D, Meda P, Durand B, Reith W: Novel function of the ciliogenic transcription factor RFX3 in development of the endocrine pancreas. Diabetes; 2007 Apr;56(4):950-9
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel function of the ciliogenic transcription factor RFX3 in development of the endocrine pancreas.
  • We show here that mouse RFX3 is expressed in developing and mature pancreatic endocrine cells during embryogenesis and in adults.
  • RFX3 expression already is evident in early Ngn3-positive progenitors and is maintained in all major pancreatic endocrine cell lineages throughout their development.
  • This ciliary abnormality is associated with a developmental defect leading to a uniquely altered cellular composition of the islets of Langerhans.
  • Just before birth, Rfx3(-/-) islets contain considerably less insulin-, glucagon-, and ghrelin-producing cells, whereas pancreatic polypeptide-positive cells are markedly increased in number.
  • In adult mice, the defect leads to small and disorganized islets, reduced insulin production, and impaired glucose tolerance.
  • These findings suggest that RFX3 participates in the mechanisms that govern pancreatic endocrine cell differentiation and that the presence of primary cilia on islet cells may play a key role in this process.
  • [MeSH-major] DNA-Binding Proteins / physiology. Islets of Langerhans / physiology. Transcription Factors / physiology

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
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  • (PMID = 17229940.001).
  • [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 / DNA-Binding Proteins; 0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 0 / TATA-Box Binding Protein; 0 / Transcription Factors; 0 / regulatory factor X transcription factors
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75. Takahashi N, Kasai H: Exocytic process analyzed with two-photon excitation imaging in endocrine pancreas. Endocr J; 2007 Jun;54(3):337-46

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exocytic process analyzed with two-photon excitation imaging in endocrine pancreas.
  • At insulin exocytosis in the pancreatic islets, it took two seconds for the fusion pore to dilate from 1.4 nm in diameter to 6 nm in diameter, and such unusual stability of the pore may be due to the crystallization of the intragranular contents.
  • [MeSH-major] Exocytosis / physiology. Islets of Langerhans / ultrastructure. Microscopy, Fluorescence, Multiphoton / methods. Secretory Vesicles / ultrastructure

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  • (PMID = 17409577.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / Insulin; 0 / SNARE Proteins; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Number-of-references] 40
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76. Wei C, Geras-Raaka E, Marcus-Samuels B, Oron Y, Gershengorn MC: Trypsin and thrombin accelerate aggregation of human endocrine pancreas precursor cells. J Cell Physiol; 2006 Feb;206(2):322-8
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  • [Title] Trypsin and thrombin accelerate aggregation of human endocrine pancreas precursor cells.
  • Because we found that hIPCs, PANC-1 cells, human fetal pancreas, and human adult islets express two protease-activated receptors (PARs), PAR-1 and PAR-2, we tested whether the effects of thrombin and trypsin were mediated, at least in part, by these receptors.
  • [MeSH-minor] Calcium / metabolism. Cell Aggregation. Cell Differentiation / drug effects. Cells, Cultured. Cytoplasm / metabolism. Humans. Islets of Langerhans / drug effects. Oligopeptides / pharmacology. RNA, Messenger / metabolism. Signal Transduction. Tumor Cells, Cultured

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  • (PMID = 16021635.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / RNA, Messenger; 0 / Receptors, Proteinase-Activated; 0 / seryl-leucyl-isoleucyl-glycyl-arginyl-leucine; EC 3.4.21.4 / Trypsin; EC 3.4.21.5 / Thrombin; SY7Q814VUP / Calcium
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77. Du A, Hunter CS, Murray J, Noble D, Cai CL, Evans SM, Stein R, May CL: Islet-1 is required for the maturation, proliferation, and survival of the endocrine pancreas. Diabetes; 2009 Sep;58(9):2059-69
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  • [Title] Islet-1 is required for the maturation, proliferation, and survival of the endocrine pancreas.
  • In this study, we tested the hypothesis that the transcriptional regulator Islet-1 (Isl-1), whose expression is first detected in the mesenchyme and epithelium of the developing pancreas and is later restricted to mature islet cells, is involved in the terminal differentiation of islet cells and maintenance of islet mass.
  • RESULTS: Isl-1-deficient endocrine precursors failed to mature into functional islet cells.
  • The postnatal expansion of endocrine cell mass was impaired, and consequently Isl-1 deficient mice were diabetic.

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  • (PMID = 19502415.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007061; United States / NIDDK NIH HHS / DK / R01 DK078606-02; United States / NIDDK NIH HHS / DK / P30 DK050306; United States / NIDDK NIH HHS / DK / P30-DK19525; United States / NIDDK NIH HHS / DK / F32 DK083160; United States / NIDDK NIH HHS / DK / R56 DK078606; United States / NIDDK NIH HHS / DK / DK083160; United States / NIDDK NIH HHS / DK / DK019525; United States / NIDDK NIH HHS / DK / P30-DK050306; United States / NIDDK NIH HHS / DK / DK007061; United States / NIDDK NIH HHS / DK / DK078606; United States / NIDDK NIH HHS / DK / DK078606-02; United States / NIDDK NIH HHS / DK / R01 DK078606; United States / NIDDK NIH HHS / DK / P30 DK019525
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / LIM-Homeodomain Proteins; 0 / Maf Transcription Factors, Large; 0 / Mafa protein, mouse; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / insulin gene enhancer binding protein Isl-1; 0 / pancreatic and duodenal homeobox 1 protein; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ PMC2731519
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78. Jäggi F, Cabrita MA, Perl AK, Christofori G: Modulation of endocrine pancreas development but not beta-cell carcinogenesis by Sprouty4. Mol Cancer Res; 2008 Mar;6(3):468-82
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  • [Title] Modulation of endocrine pancreas development but not beta-cell carcinogenesis by Sprouty4.
  • Here, by the inducible expression of murine Spry4 in pancreatic beta cells, we have assessed the functional role of Spry proteins in the development of pancreatic islets of Langerhans in normal mice and in the Rip1Tag2 transgenic mouse model of beta-cell carcinogenesis. beta cell-specific expression of mSpry4 provokes a significant reduction in islet size, an increased number of alpha cells per islet area, and impaired islet cell type segregation.
  • Functional analysis of islet cell differentiation in cultured PANC-1 cells shows that mSpry4 represses adhesion and migration of differentiating pancreatic endocrine cells, most likely by affecting the subcellular localization of the protein tyrosine phosphatase PTP1B.
  • In contrast, transgenic expression of mSpry4 during beta-cell carcinogenesis does not significantly affect tumor outgrowth and progression to tumor malignancy.
  • Rather, tumor cells seem to escape mSpry4 transgene expression.
  • [MeSH-major] Insulin-Secreting Cells / physiology. Islets of Langerhans / physiology. Nerve Tissue Proteins / physiology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA Primers. Disease Progression. Gene Expression Regulation, Neoplastic. Glucose Tolerance Test. Humans. Mice. Mice, Inbred C57BL. Mice, Transgenic. Nuclear Pore Complex Proteins / genetics. Polymerase Chain Reaction. RNA-Binding Proteins / genetics. Receptor Protein-Tyrosine Kinases / metabolism. Signal Transduction

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  • (PMID = 18337453.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AGFG1 protein, human; 0 / DNA Primers; 0 / Nerve Tissue Proteins; 0 / Nuclear Pore Complex Proteins; 0 / RNA-Binding Proteins; 0 / Spry4 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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79. Collombat P, Hecksher-Sørensen J, Krull J, Berger J, Riedel D, Herrera PL, Serup P, Mansouri A: Embryonic endocrine pancreas and mature beta cells acquire alpha and PP cell phenotypes upon Arx misexpression. J Clin Invest; 2007 Apr;117(4):961-70
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  • [Title] Embryonic endocrine pancreas and mature beta cells acquire alpha and PP cell phenotypes upon Arx misexpression.
  • To establish whether Arx is not only necessary, but also sufficient to instruct the alpha cell fate in endocrine progenitors, we used a gain-of-function approach to generate mice conditionally misexpressing this factor.
  • Mice with forced Arx expression in the embryonic pancreas or in developing islet cells developed a dramatic hyperglycemia and eventually died.
  • These results provide important insights into the complex mechanisms underlying proper pancreatic endocrine cell allocation and cell identity acquisition.

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  • (PMID = 17404619.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / U19 DK072495; United States / NIDDK NIH HHS / DK / U19 DK072495-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARX protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors; 59763-91-6 / Pancreatic Polypeptide; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ PMC1839241
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80. da Silva CA, Cancelliero KM, Costa D: The effect of chemical therapy with bleomycin sulfate on the functional parameters of the endocrine pancreas. JOP; 2009;10(3):292-8
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  • [Title] The effect of chemical therapy with bleomycin sulfate on the functional parameters of the endocrine pancreas.
  • OBJECTIVE: The objective of the present study was to evaluate the effect of bleomycin sulfate on parameters related to the functionality of pancreatic tissue, with emphasis on the glucose tolerance test, insulin tolerance test, insulinemia and static secretion of insulin as well as the insulin receptor, and PKA, PKC and GLUT2 concentrations in the pancreatic islets.
  • With respect to the concentrations of the insulin receptor, GLUT2, PKC and PKA in the pancreatic islets of the bleomycin group, there was an increase in GLUT2 (48.4%) and PKC (70.8%) and a reduction in PKA (38.5%).
  • [MeSH-major] Antibiotics, Antineoplastic / toxicity. Bleomycin / toxicity. Islets of Langerhans / drug effects. Pancreatic Diseases / chemically induced

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  • (PMID = 19454822.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Glucose Transporter Type 2; 0 / Insulin; 0 / Slc2a2 protein, rat; 11056-06-7 / Bleomycin; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.13 / Protein Kinase C
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81. Avnit-Sagi T, Kantorovich L, Kredo-Russo S, Hornstein E, Walker MD: The promoter of the pri-miR-375 gene directs expression selectively to the endocrine pancreas. PLoS One; 2009;4(4):e5033
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The promoter of the pri-miR-375 gene directs expression selectively to the endocrine pancreas.
  • The aim of this study was to elucidate the molecular basis of cell-specific expression of the pri-miR-375 gene, which is selectively expressed in pancreatic islets, and has been implicated both in the development of islets, and the function of mature pancreatic beta cells.
  • The conserved 768 bp region was able to direct preferential expression of a GFP reporter gene to pancreatic islets in transgenic mice.
  • [MeSH-major] Gene Expression Regulation / genetics. Islets of Langerhans / metabolism. MicroRNAs / genetics. Promoter Regions, Genetic

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  • (PMID = 19343226.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Complementary; 0 / MicroRNAs; 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ PMC2660411
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82. Cheng H, Wolfe SH, Valencia V, Qian K, Shen L, Phillips MI, Chang LJ, Zhang YC: Efficient and persistent transduction of exocrine and endocrine pancreas by adeno-associated virus type 8. J Biomed Sci; 2007 Sep;14(5):585-94
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  • [Title] Efficient and persistent transduction of exocrine and endocrine pancreas by adeno-associated virus type 8.
  • Efficient delivery of therapeutic proteins into the pancreas represents a major obstacle to gene therapy of pancreatic disorders.
  • Our results indicate that lentivirus and AAV 1, 2, 8 are capable of transducing pancreas with the order of efficiency AAV8 >>AAV1 > AAV2 >/= lentivirus, whereas AAV5 was ineffective.
  • AAV8 resulted in an efficient, persistent (150 days) and dose-dependent transduction in exocrine acinar cells and endocrine islet cells.
  • Leukocyte infiltration was not observed in pancreas and blood glucose levels were not altered.
  • Thus, AAV8 represents a safe and effective vehicle for therapeutic gene transfer to pancreas in vivo.
  • [MeSH-major] Dependovirus / genetics. Genetic Therapy. Genetic Vectors / genetics. Islets of Langerhans. Pancreas, Exocrine

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  • (PMID = 17387636.001).
  • [ISSN] 1021-7770
  • [Journal-full-title] Journal of biomedical science
  • [ISO-abbreviation] J. Biomed. Sci.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL067248
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Blood Glucose; 147336-22-9 / Green Fluorescent Proteins
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83. Roche E, Santana A, Vicente-Salar N, Reig JA: From stem cells to insulin-producing cells: towards a bioartificial endocrine pancreas. Panminerva Med; 2005 Mar;47(1):39-51
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  • [Title] From stem cells to insulin-producing cells: towards a bioartificial endocrine pancreas.
  • However, transplantation trials for diabetes have to face the scarcity of islets from cadaveric donors.
  • These criteria concern to the type of stem cell to be used as starting biomaterial (embryonic or adult), the in vitro differentiation protocol applied, the functional phenotype reached for the final cell product and the transplantation associated problems (likely immune rejection and tumor formation).
  • [MeSH-major] Bioartificial Organs. Cell Differentiation. Insulin / biosynthesis. Pancreas, Artificial. Stem Cells / cytology. Stem Cells / metabolism

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  • (PMID = 15985976.001).
  • [ISSN] 0031-0808
  • [Journal-full-title] Panminerva medica
  • [ISO-abbreviation] Panminerva Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Insulin
  • [Number-of-references] 72
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84. Davies SL, Best L, Brown PD: HCO 3--dependent volume regulation in alpha-cells of the rat endocrine pancreas. Pflugers Arch; 2009 Jul;458(3):621-9
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  • [Title] HCO 3--dependent volume regulation in alpha-cells of the rat endocrine pancreas.
  • [MeSH-minor] Animals. Cell Size / drug effects. Cells, Cultured. Islets of Langerhans / cytology. Islets of Langerhans / drug effects. Islets of Langerhans / physiology. Male. Rats. Rats, Sprague-Dawley

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  • (PMID = 19214560.001).
  • [ISSN] 1432-2013
  • [Journal-full-title] Pflügers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bicarbonates
  • [Other-IDs] NLM/ PMC2691524
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85. Wilson ME, Yang KY, Kalousova A, Lau J, Kosaka Y, Lynn FC, Wang J, Mrejen C, Episkopou V, Clevers HC, German MS: The HMG box transcription factor Sox4 contributes to the development of the endocrine pancreas. Diabetes; 2005 Dec;54(12):3402-9
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  • [Title] The HMG box transcription factor Sox4 contributes to the development of the endocrine pancreas.
  • To investigate the role of the Sry/hydroxymethylglutaryl box (Sox) transcription factors in the development of the pancreas, we determined the expression pattern of Sox factors in the developing mouse pancreas.
  • By RT-PCR, we detected the presence of multiple Sox family members in both the developing pancreas and mature islets and then focused on two factors, Sox2 and Sox4.
  • Mice homozygous for a null mutation of the sox4 gene showed normal pancreatic bud formation and endocrine cell differentiation up to embryonic day 12.5.
  • Beyond that date, cultured pancreatic explants lacking sox4 failed to form normal islets.
  • Instead, a markedly reduced number of endocrine cells were found scattered through the explant.
  • We show here that several Sox transcription factors are expressed in the developing pancreas and in the islet, and that one of these factors, Sox4, is required for the normal development of pancreatic islets.
  • [MeSH-major] High Mobility Group Proteins / genetics. Islets of Langerhans / physiology. Trans-Activators / genetics
  • [MeSH-minor] Animals. DNA Primers. DNA-Binding Proteins / deficiency. Ectoderm / physiology. Gene Expression Regulation, Developmental. HMG-Box Domains. Male. Mice. Mice, Knockout. Nuclear Proteins / deficiency. Pancreas / embryology. Pancreas / physiology. Reverse Transcriptase Polymerase Chain Reaction. SOXC Transcription Factors. SOXD Transcription Factors. Sex-Determining Region Y Protein / metabolism

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  • (PMID = 16306355.001).
  • [ISSN] 0012-1797
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U120074332; United States / NIDDK NIH HHS / DK / DK2134; United States / NIDDK NIH HHS / DK / DK61245; United States / NIDDK NIH HHS / DK / P30 DK063720
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / High Mobility Group Proteins; 0 / Nuclear Proteins; 0 / SOXC Transcription Factors; 0 / SOXD Transcription Factors; 0 / Sex-Determining Region Y Protein; 0 / Sox4 protein, mouse; 0 / Sox5 protein, mouse; 0 / Trans-Activators
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86. Gupta S, McGrath B, Cavener DR: PERK regulates the proliferation and development of insulin-secreting beta-cell tumors in the endocrine pancreas of mice. PLoS One; 2009 Nov 24;4(11):e8008
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  • [Title] PERK regulates the proliferation and development of insulin-secreting beta-cell tumors in the endocrine pancreas of mice.
  • Tumor growth and the related parameters of cell proliferation were measured.
  • Beta-cell proliferation was ablated in Perk-deficient mice associated with reduced tumor growth.
  • In the small number of large encapsulated insulinomas that developed in Perk-deficient mice, we found a dramatic reduction in tumor vascularity compared to similar sized insulinomas in wild-type mice.

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  • (PMID = 19956728.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062049; United States / NIGMS NIH HHS / GM / R01 GM056957; United States / NIDDK NIH HHS / DK / R01-DK062049; United States / NIGMS NIH HHS / GM / R01-GM56957
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / Blood Glucose; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / eIF-2 Kinase
  • [Other-IDs] NLM/ PMC2776514
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87. Foo KS, Brauner H, Ostenson CG, Broberger C: Nucleobindin-2/nesfatin in the endocrine pancreas: distribution and relationship to glycaemic state. J Endocrinol; 2010 Mar;204(3):255-63
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  • [Title] Nucleobindin-2/nesfatin in the endocrine pancreas: distribution and relationship to glycaemic state.
  • Given the overlap of signalling molecules between the brain and pancreas, we have explored the presence of NUCB2 in the islets of Langerhans.
  • NUCB2-like immunoreactivity was detected by immunofluorescence in all human and rat islet beta-cells (as detected by co-localization with insulin), but not in other islet cells or in the exocrine pancreas.
  • Islet NUCB2 content, as measured by enzyme immunoassay, did not change significantly following an overnight fast, but was substantially lower in islets isolated from an animal model of type 2 diabetes, the Goto-Kakizaki (GK) rats (48% of non-diabetic Wistar rat control).
  • The release of NUCB2 from isolated rat islets was significantly elevated following glucose challenge (123%), but this effect was substantially lower than that observed for insulin (816%).
  • However, our findings, together with previous reports, appear more compatible with intracellular actions rather than with endocrine/paracrine communication, and suggest that NUCB2 in serum derives primarily from non-islet sources.
  • [MeSH-major] Calcium-Binding Proteins / metabolism. DNA-Binding Proteins / metabolism. Glucose / metabolism. Islets of Langerhans / metabolism


88. Chandavar VR, Naik PR: Immunocytochemical detection of glucagon and insulin cells in endocrine pancreas and cyclic disparity of plasma glucose in the turtle Melanochelys trijuga. J Biosci; 2008 Jun;33(2):239-47
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  • [Title] Immunocytochemical detection of glucagon and insulin cells in endocrine pancreas and cyclic disparity of plasma glucose in the turtle Melanochelys trijuga.
  • Pancreatic endocrine cells were immunochemically localized.Insulin-immunoreactive (IR) cells occurred in groups of 3-20 and were in close apposition, while glucagon-IR cells were distributed individually between the exocrine pancreas or formed anastomosing cords where cells were not intimately attached.
  • Glucagon-IR cells seemed to be secretory throughout the pancreas during the reproductive cycle,while insulin-IR cells were found to be pulsating in their secretion.
  • [MeSH-major] Blood Glucose / metabolism. Glucagon / metabolism. Insulin / metabolism. Islets of Langerhans / metabolism. Turtles / metabolism

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  • (PMID = 18535358.001).
  • [ISSN] 0250-5991
  • [Journal-full-title] Journal of biosciences
  • [ISO-abbreviation] J. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 9007-92-5 / Glucagon
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89. Itoh M, Takizawa Y, Hanai S, Okazaki S, Miyata R, Inoue T, Akashi T, Hayashi M, Goto Y: Partial loss of pancreas endocrine and exocrine cells of human ARX-null mutation: consideration of pancreas differentiation. Differentiation; 2010 Sep-Oct;80(2-3):118-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Partial loss of pancreas endocrine and exocrine cells of human ARX-null mutation: consideration of pancreas differentiation.
  • Since ARX expresses in the islets of Langerhans during the embryonic stage, these visceral phenotypes may be related to a loss of ARX function, which develops endocrine cells in the pancreas.
  • We performed immunohistochemistry of XLAG pancreases, using the antibodies against glucagon, insulin, somatostatin, pancreatic polypeptide, ghrelin, Brn4, Nkx2.2, Mash1, amylase and pancreatic lipase.
  • As the results, the glucagon- and pancreatic polypeptide-producing cells were found to be completely deficient in the islets of Langerhans.
  • These pathological findings indicate that ARX contributes not only to endocrine development, but also to exocrine development of the human pancreas, and its deficiency may lead to the severe phenotypes of XLAG patients.
  • [MeSH-major] Cell Differentiation. Homeodomain Proteins / genetics. Islets of Langerhans / embryology. Mutation. Transcription Factors / genetics

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  • [Copyright] Copyright © 2010 International Society of Differentiation. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20538404.001).
  • [ISSN] 1432-0436
  • [Journal-full-title] Differentiation; research in biological diversity
  • [ISO-abbreviation] Differentiation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ARX protein, human; 0 / Homeodomain Proteins; 0 / Transcription Factors
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90. Hettiarachchi KD, Zimmet PZ, Danial NN, Myers MA: Transplacental exposure to the vacuolar-ATPase inhibitor bafilomycin disrupts survival signaling in beta cells and delays neonatal remodeling of the endocrine pancreas. Exp Toxicol Pathol; 2008 Aug;60(4-5):295-306
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  • [Title] Transplacental exposure to the vacuolar-ATPase inhibitor bafilomycin disrupts survival signaling in beta cells and delays neonatal remodeling of the endocrine pancreas.
  • Bafilomycin exposure also inactivated the insulin/IGF signaling pathway intermediate, FoxO1, and increased the insulin content in neonatal islets.
  • [MeSH-major] Enzyme Inhibitors / toxicity. Insulin-Secreting Cells / drug effects. Islets of Langerhans / drug effects. Macrolides / toxicity. Prenatal Exposure Delayed Effects / physiopathology
  • [MeSH-minor] Animals. Animals, Newborn. Apoptosis / drug effects. Blotting, Western. Cell Survival / drug effects. Female. Fluorescent Antibody Technique. Forkhead Transcription Factors / drug effects. In Situ Nick-End Labeling. Insulin / biosynthesis. Mice. Mice, Inbred C57BL. Phosphorylation. Polymerase Chain Reaction. Pregnancy. Signal Transduction / drug effects. bcl-Associated Death Protein / biosynthesis. bcl-Associated Death Protein / drug effects

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  • (PMID = 18486461.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bad protein, mouse; 0 / Enzyme Inhibitors; 0 / Forkhead Transcription Factors; 0 / Foxo1 protein, mouse; 0 / Insulin; 0 / Macrolides; 0 / bcl-Associated Death Protein; 88899-56-3 / bafilomycin B1
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91. Nagasao J, Yoshioka K, Amasaki H, Tsujio M, Ogawa M, Taniguchi K, Mutoh K: Morphological changes in the rat endocrine pancreas within 12 h of intravenous streptozotocin administration. Anat Histol Embryol; 2005 Feb;34(1):42-7
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  • [Title] Morphological changes in the rat endocrine pancreas within 12 h of intravenous streptozotocin administration.
  • We examined early morphological changes in pancreatic endocrine cells within 12 h of intravenous streptozotocin (STZ) administration (60 mg/kg).
  • [MeSH-major] Blood Glucose / metabolism. Diabetes Mellitus, Experimental / pathology. Insulin / metabolism. Islets of Langerhans / pathology

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  • (PMID = 15649226.001).
  • [ISSN] 0340-2096
  • [Journal-full-title] Anatomia, histologia, embryologia
  • [ISO-abbreviation] Anat Histol Embryol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 5W494URQ81 / Streptozocin
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92. Ritz-Laser B, Mamin A, Brun T, Avril I, Schwitzgebel VM, Philippe J: The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression. Mol Endocrinol; 2005 Mar;19(3):759-70
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  • [Title] The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression.
  • We show here that Gata-4 and/or Gata-6 are not only expressed in the adult exocrine pancreas but also in glucagonoma and insulinoma cell lines, whereas Gata-5 is restricted to the exocrine pancreas.
  • During pancreas development, Gata-4 is expressed already at embryonic d 10.5 and colocalizes with early glucagon+ cells at embryonic d 12.5.
  • We conclude that, besides its role in endoderm differentiation, Gata-4 might be implicated in the regulation of glucagon gene expression in the fetal pancreas and that Gata activity itself may be modulated by interactions with different cofactors.
  • [MeSH-major] DNA-Binding Proteins / chemistry. Gene Expression Regulation. Glucagon / metabolism. Islets of Langerhans / metabolism. Transcription Factors / chemistry. Zinc Fingers
  • [MeSH-minor] Animals. Base Sequence. Binding Sites. Cell Differentiation. Cell Line. Cell Nucleus / metabolism. Chloramphenicol O-Acetyltransferase / metabolism. Cricetinae. Dose-Response Relationship, Drug. GATA4 Transcription Factor. GATA6 Transcription Factor. Humans. Mice. Microscopy, Fluorescence. Molecular Sequence Data. Mutation. Pancreas / embryology. Promoter Regions, Genetic. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tissue Distribution. Transcriptional Activation. Transfection


93. Moriscot C, de Fraipont F, Richard MJ, Marchand M, Savatier P, Bosco D, Favrot M, Benhamou PY: Human bone marrow mesenchymal stem cells can express insulin and key transcription factors of the endocrine pancreas developmental pathway upon genetic and/or microenvironmental manipulation in vitro. Stem Cells; 2005 Apr;23(4):594-603
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  • [Title] Human bone marrow mesenchymal stem cells can express insulin and key transcription factors of the endocrine pancreas developmental pathway upon genetic and/or microenvironmental manipulation in vitro.
  • Our goal was to characterize the multipotential capacities of human mesenchymal stem cells (hMSCs) and to evaluate their ability to differentiate into insulin-secreting cells in vitro. hMSCs were obtained from healthy donors, selected by plastic adhesion, and phenotyped by fluorescence-activated cell sorter and reverse transcription-polymerase chain reaction analysis before and after infection with adenoviruses coding for mouse IPF1, HLXB9, and FOXA2 transcription factors involved early in the endocrine developmental pathway.

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  • (PMID = 15790780.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Foxa2 protein, mouse; 0 / Homeodomain Proteins; 0 / Insulin; 0 / NKX6-1 protein, human; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta; 140115-73-7 / Hb9 protein, mouse
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94. Egerod KL, Holst B, Petersen PS, Hansen JB, Mulder J, Hökfelt T, Schwartz TW: GPR39 splice variants versus antisense gene LYPD1: expression and regulation in gastrointestinal tract, endocrine pancreas, liver, and white adipose tissue. Mol Endocrinol; 2007 Jul;21(7):1685-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GPR39 splice variants versus antisense gene LYPD1: expression and regulation in gastrointestinal tract, endocrine pancreas, liver, and white adipose tissue.
  • Quantitative RT-PCR analysis demonstrated that GPR39-1a is expressed selectively throughout the gastrointestinal tract, including the liver and pancreas as well as in the kidney and adipose tissue, whereas the truncated GPR39-1b form has a more broad expression pattern, including the central nervous system but with highest expression in the stomach and small intestine.
  • It is concluded that the transcriptional control mechanism, the tissue expression pattern, and in vivo response to physiological stimuli all indicate that the GPR39 receptor very likely is of importance for the function of a number of metabolic organs, including the liver, gastrointestinal tract, pancreas, and adipose tissue.
  • [MeSH-minor] Adipose Tissue / metabolism. Adipose Tissue, Brown / metabolism. Alternative Splicing. Amino Acid Sequence. Animals. Base Sequence. Cell Line. DNA Primers / genetics. Diabetes Mellitus, Experimental / genetics. Diabetes Mellitus, Experimental / metabolism. Gastrointestinal Tract / metabolism. Gene Expression Regulation. Humans. In Situ Hybridization. Islets of Langerhans / metabolism. Liver / metabolism. Male. Models, Molecular. Molecular Sequence Data. Promoter Regions, Genetic. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Tissue Distribution

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  • (PMID = 17488974.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antisense Elements (Genetics); 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled
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95. Protzek AO, Rafacho A, Viscelli BA, Bosqueiro JR, Cappelli AP, Paula FM, Boschero AC, Pinheiro EC: Insulin and glucose sensitivity, insulin secretion and beta-cell distribution in endocrine pancreas of the fruit bat Artibeus lituratus. Comp Biochem Physiol A Mol Integr Physiol; 2010 Oct;157(2):142-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insulin and glucose sensitivity, insulin secretion and beta-cell distribution in endocrine pancreas of the fruit bat Artibeus lituratus.
  • Based on these data, we aimed to investigate various aspects related with glucose homeostasis analyzing: blood glucose and insulin levels, intraperitoneal glucose and insulin tolerance tests (ipGTT and ipITT), glucose-stimulated insulin secretion (2.8, 5.6 or 8.3 mmol/L glucose) in pancreas fragments, cellular distribution of beta cells, and the amount of pAkt/Akt in the pectoral muscle and liver.
  • Insulin secretion from fragments of pancreas under physiological concentrations of glucose (5.6 or 8.3 mmol/L) was similar but higher than in 2.8 mmol/L glucose 1.8- and 2.0-fold, respectively.
  • These bats showed a marked beta-cell distribution along the pancreas, and the pancreatic beta cells are not exclusively located at the central part of the islet.

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20566319.001).
  • [ISSN] 1531-4332
  • [Journal-full-title] Comparative biochemistry and physiology. Part A, Molecular & integrative physiology
  • [ISO-abbreviation] Comp. Biochem. Physiol., Part A Mol. Integr. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; IY9XDZ35W2 / Glucose
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96. Kaczmarek P, Malendowicz LK, Pruszynska-Oszmalek E, Wojciechowicz T, Szczepankiewicz D, Szkudelski T, Nowak KW: Neuromedin U receptor 1 expression in the rat endocrine pancreas and evidence suggesting neuromedin U suppressive effect on insulin secretion from isolated rat pancreatic islets. Int J Mol Med; 2006 Nov;18(5):951-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuromedin U receptor 1 expression in the rat endocrine pancreas and evidence suggesting neuromedin U suppressive effect on insulin secretion from isolated rat pancreatic islets.
  • Therefore in the present study we examined the expression of NmU receptors in pancreatic islets using RT-PCR and Western blotting analysis.
  • We also investigated the role of NmU in regulation of insulin secretion in vitro using isolated pancreatic islets.
  • We have confirmed that NmUR1 but not NmUR2 is specifically expressed in isolated rat pancreatic islets.
  • In all tested doses (1, 10, 100 nmol/l) NmU dose- dependently decreased insulin output by isolated pancreatic islets.
  • [MeSH-major] Appetite Depressants / pharmacology. Insulin / secretion. Insulin Antagonists / pharmacology. Islets of Langerhans / drug effects. Membrane Proteins / metabolism. Neuropeptides / pharmacology. Receptors, Neurotransmitter / metabolism


97. Devlieger R, Casteels K, Van Assche FA: Reduced adaptation of the pancreatic B cells during pregnancy is the major causal factor for gestational diabetes: current knowledge and metabolic effects on the offspring. Acta Obstet Gynecol Scand; 2008;87(12):1266-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This commentary summarizes current knowledge on the pathophysiology of gestational diabetes, focusing on the role of the endocrine pancreas and the beta-cells, their adaptation in normal pregnancy, and recent insights in the molecular basis for deficient adaptation in diabetes occurring during pregnancy.

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  • (PMID = 18846453.001).
  • [ISSN] 1600-0412
  • [Journal-full-title] Acta obstetricia et gynecologica Scandinavica
  • [ISO-abbreviation] Acta Obstet Gynecol Scand
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin
  • [Number-of-references] 37
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98. Thorens B: Central control of glucose homeostasis: the brain--endocrine pancreas axis. Diabetes Metab; 2010 Oct;36 Suppl 3:S45-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Central control of glucose homeostasis: the brain--endocrine pancreas axis.
  • A large body of data gathered over the last decades has delineated the neuronal pathways that link the central nervous system with the autonomic innervation of the endocrine pancreas, which controls alpha- and beta-cell secretion activity and mass.
  • These are important regulatory functions that are certainly keys for preserving the capacity of the endocrine pancreas to control glucose homeostasis over a lifetime.
  • Identifying the cells involved in controlling the autonomic innervation of the endocrine pancreas, in response to nutrient, hormonal and environmental cues and how these cues are detected to activate neuronal activity are important goals of current research.

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 21211735.001).
  • [ISSN] 1878-1780
  • [Journal-full-title] Diabetes & metabolism
  • [ISO-abbreviation] Diabetes Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Insulin; 9007-92-5 / Glucagon; IY9XDZ35W2 / Glucose
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99. Engler D: Hypothesis: Musculin is a hormone secreted by skeletal muscle, the body's largest endocrine organ. Evidence for actions on the endocrine pancreas to restrain the beta-cell mass and to inhibit insulin secretion and on the hypothalamus to co-ordinate the neuroendocrine and appetite responses to exercise. Acta Biomed; 2007;78 Suppl 1:156-206
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  • [Title] Hypothesis: Musculin is a hormone secreted by skeletal muscle, the body's largest endocrine organ. Evidence for actions on the endocrine pancreas to restrain the beta-cell mass and to inhibit insulin secretion and on the hypothalamus to co-ordinate the neuroendocrine and appetite responses to exercise.
  • Recent studies indicate that skeletal muscle may act as an endocrine organ by secreting interleukin-6 (IL-6) into the systemic circulation.

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  • (PMID = 17465332.001).
  • [ISSN] 0392-4203
  • [Journal-full-title] Acta bio-medica : Atenei Parmensis
  • [ISO-abbreviation] Acta Biomed
  • [Language] eng
  • [Publication-type] Lectures
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Hormones; 0 / Insulin; 0 / Interleukin-5; 0 / Neuropeptides; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; IY9XDZ35W2 / Glucose
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100. El Idrissi A, Boukarrou L, L'Amoreaux W: Taurine supplementation and pancreatic remodeling. Adv Exp Med Biol; 2009;643:353-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study we evaluated the role of taurine in pancreatic islets development, since the endocrine pancreas undergoes significant modifications during neonatal life.
  • Histological examination of the pancreas from taurine-fed mice revealed no histological abnormalities in the endocrine or exocrine parts of the pancreas.
  • However, supplementation of taurine in the drinking water resulted in a drastic and significant increase in the number of islets per section.
  • Furthermore, islets size was significantly larger.
  • We hypothesize that supplementation of taurine, which is important for the development of the endocrine pancreas may reduce cytokine-induced apoptosis in pancreatic beta cells.
  • The endocrine pancreas undergoes significant modifications during neonatal life and apoptosis is an important mechanism in this remodeling.
  • We suggest that alteration of this remodeling process during this period of time, when a fine balance between cell replication and cell death is critical, would affect the development of the pancreatic islets of Langerhans, and could have important effects on the pancreatic cell mass and the endocrine function.
  • [MeSH-major] Dietary Supplements. Pancreas / drug effects. Taurine / administration & dosage

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  • (PMID = 19239166.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 1EQV5MLY3D / Taurine
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