2015 Fiscal Year Final Research Report
Functional Analysis of PI3K and GLP-1 in pancreatic beta cells.
| Project/Area Number |
26860689
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | 糖尿病 / 膵β細胞 / GLP-1 |
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| Outline of Final Research Achievements |
Deletion of class IA phosphatidylinositol 3-kinase (PI3K), using a mouse model lacking the pik3r1 gene specifically in β cells and the pik3r2 gene (bDKO mouse) results in glucose intolerance and reduced early insulin secretion. Glucose intolerance has not been alleviated with administration of GLP-1 analog in bDKO mice. Microarray analysis showed the expression of epidermal growth factor receptor (EGFR). EGFR is reported to be necessary to act GLP-1 analog through betacellulin, EGFR agonist. EGFR expression in islets is suppressed in diabetic DB/DB mice. EGFR is regulated by AKT/Foxo1 pathway in vitro model. This result indicated that EGFR, regulated by PI3K AKT/ Foxo1 pathway in pancreatic β cells, is important for GLP-1 signaling.
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| Free Research Field |
医歯薬学
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