| Exendin-4, a glucagon-like peptide-1 receptor agonist, inhibits cell apoptosis induced by lipotoxicity in pancreatic β-cell line. | |
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MedLine Citation:
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PMID: 22776329 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Lipotoxicity plays an important role in the underlying mechanism of type 2 diabetes mellitus. Prolonged exposure of pancreatic β-cells to elevated concentrations of fatty acid is associated with β-cell apoptosis. Recently, glucagon-like peptide-1 (GLP-1) receptor agonists have been reported to have direct beneficial effects on β-cells, such as anti-apoptotic effects, increased β-cell mass, and improvement of β-cell function. The mechanism of GLP-1 receptor agonists' protection of pancreatic β-cells against lipotoxicity is not completely understood. We investigated whether the GLP-1 receptor agonist exendin-4 promoted cell survival and attenuated palmitate-induced apoptosis in murine pancreatic β-cells (MIN6). Exposure of MIN6 cells to palmitate (0.4mM) for 24h caused a significant increase in cell apoptosis, which was inhibited by exendin-4. Exposure of MIN6 cells to exendin-4 caused rapid activation of protein kinase B (PKB) under lipotoxic conditions. Furthermore, LY294002, a PI3K inhibitor, abolished the anti-lipotoxic effect of exendin-4 on MIN6 cells. Exendin-4 also inhibited the mitochondrial pathway of apoptosis and down-regulated Bax in MIN6 cells. Exendin-4 enhanced glucose-stimulated insulin secretion in the presence of palmitate. Our findings suggest that exendin-4 may prevent lipotoxicity-induced apoptosis in MIN6 cells through activation of PKB and inhibition of the mitochondrial pathway. |
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Authors:
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Qian Wei; Yu Qiang Sun; Jin Zhang |
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Publication Detail:
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Type: Journal Article Date: 2012-07-07 |
Journal Detail:
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Title: Peptides Volume: 37 ISSN: 1873-5169 ISO Abbreviation: Peptides Publication Date: 2012 Sep |
Date Detail:
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Created Date: 2012-08-24 Completed Date: 2013-01-07 Revised Date: 2013-03-19 |
Medline Journal Info:
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Nlm Unique ID: 8008690 Medline TA: Peptides Country: United States |
Other Details:
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Languages: eng Pagination: 18-24 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Endocrinology, The First Affiliated Hospital of China Medical University, No. 155, Nanjing North Street, Heping District, Shenyang, Liaoning 110001, China. weiqianinsy@gmail.com |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects* Cell Survival / drug effects Cells, Cultured Cytoprotection Insulin / secretion Insulin-Secreting Cells / drug effects*, physiology, secretion Mice Mitochondria / drug effects, metabolism Palmitates / toxicity* Peptides / pharmacology* Phosphatidylinositol 3-Kinases / metabolism Proto-Oncogene Proteins c-akt / metabolism Proto-Oncogene Proteins c-bcl-2 / metabolism Receptors, Glucagon / agonists*, metabolism Signal Transduction Venoms / pharmacology* bcl-2-Associated X Protein / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Bax protein, mouse; 0/Insulin; 0/Palmitates; 0/Peptides; 0/Proto-Oncogene Proteins c-bcl-2; 0/Receptors, Glucagon; 0/Venoms; 0/bcl-2-Associated X Protein; 0/glucagon-like peptide-1 receptor; 141732-76-5/exenatide; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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