Functional Analysis of PI3K and GLP-1 in pancreatic beta cells.
| Project/Area Number |
26860689
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Metabolomics
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| 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)
|
|---|
| Keywords | 糖尿病 / 膵β細胞 / GLP-1 / egfr / インスリンシグナル |
|---|
| 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.
|
Report
(3 results)
Research Products
(7 results)
