Short-form GIP; Its Secretion and Glucose homeostasis
Project/Area Number |
23591291
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | Asahikawa Medical College |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
HONJO Jun 旭川医科大学, 内科学講座病態代謝内科学分野, 特任助教 (30451462)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | GIP / インクレチン / 膵島 / α細胞 / 糖尿病 |
Research Abstract |
GIP is an incretin hormone, which is released from the gut and involved in homeostasis of glucose metabolism though glucose-depedent insulin secretion from pancreatic beta cells. Interestingly, c-terminal truncated short-form GIP is expressed in pancreatic alpha cells. We found expanded short-from GIP expression in the islet of several diabetic animal models. We synthesized modified short-form GIP and confirmed the peptide to be biologically active by the administration to the normal mice. Finally we treated STZ induced diabetic mice with modified short-form GIP and observed the peptide showed potential to suppress the progression to chronic hyperglycemia in the diabetic model.
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Report
(4 results)
Research Products
(18 results)