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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2010-11-9
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pubmed:abstractText |
Oxidative stress induced by chronic hyperglycemia in type 2 diabetes plays a crucial role in progressive loss of ?-cell mass through ?-cell apoptosis. Glucagon like peptide-1 (GLP-1) has effects on preservation of ?-cell mass and its insulin secretory function. GLP-1 possibly increases islet cell mass through stimulated proliferation from ?-cell and differentiation to ?-cell from progenitor cells. Also, it probably has an antiapoptotic effect on ?-cell, but detailed mechanisms are not proven. Therefore, we examined the protective mechanism of GLP-1 in ?-cell after induction of oxidative stress. The cell apoptosis decreased to ~50% when cells were treated with 100 µM H(2)O(2) for up to 2 hr. After pretreatment of Ex-4, GLP-1 receptor agonist, flow cytometric analysis shows 41.7% reduction of ?-cell apoptosis. This data suggested that pretreatment of Ex-4 protect from oxidative stress-induced apoptosis. Also, Ex-4 treatment decreased GSK3? activation, JNK phosphorylation and caspase-9, -3 activation and recovered the expression of insulin2 mRNA in ?-cell lines and secretion of insulin in human islet. These results suggest that Ex-4 may protect ?-cell apoptosis by blocking the JNK and GSK3? mediated apoptotic pathway.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon-Like Peptide 1,
http://linkedlifedata.com/resource/pubmed/chemical/Glycogen Synthase Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Peroxide,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/JNK Mitogen-Activated Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glucagon,
http://linkedlifedata.com/resource/pubmed/chemical/Venoms,
http://linkedlifedata.com/resource/pubmed/chemical/exenatide,
http://linkedlifedata.com/resource/pubmed/chemical/glucagon-like peptide receptor,
http://linkedlifedata.com/resource/pubmed/chemical/glycogen synthase kinase 3 beta
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1598-6357
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1626-32
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21060752-Animals,
pubmed-meshheading:21060752-Apoptosis,
pubmed-meshheading:21060752-Caspase 3,
pubmed-meshheading:21060752-Caspase 9,
pubmed-meshheading:21060752-Cells, Cultured,
pubmed-meshheading:21060752-Cricetinae,
pubmed-meshheading:21060752-Flow Cytometry,
pubmed-meshheading:21060752-Glucagon-Like Peptide 1,
pubmed-meshheading:21060752-Glycogen Synthase Kinase 3,
pubmed-meshheading:21060752-Humans,
pubmed-meshheading:21060752-Hydrogen Peroxide,
pubmed-meshheading:21060752-Insulin,
pubmed-meshheading:21060752-Insulin-Secreting Cells,
pubmed-meshheading:21060752-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:21060752-Oxidative Stress,
pubmed-meshheading:21060752-Peptides,
pubmed-meshheading:21060752-Phosphorylation,
pubmed-meshheading:21060752-Receptors, Glucagon,
pubmed-meshheading:21060752-Signal Transduction,
pubmed-meshheading:21060752-Venoms
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pubmed:year |
2010
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pubmed:articleTitle |
Exendin-4 protects oxidative stress-induced ?-cell apoptosis through reduced JNK and GSK3? activity.
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pubmed:affiliation |
Division of Endocrinology and Metabolism, Department of Internal Medicine, Konyang University School of Medicine, Daejeon, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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