| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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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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