| Project/Area Number |
20591070
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
|
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| Research Institution | Jichi Medical University |
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Principal Investigator |
DEZAKI Katsuya Jichi Medical University, 医学部, 准教授 (90337329)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YADA Toshihiko 自治医科大学, 医学部, 教授 (60166527)
|
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
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| Keywords | 生理学 / 糖尿病 / インスリン分泌 / シグナル伝達 |
|---|
| Research Abstract |
Ghrelin, an acylated 28-amino acid peptide, was isolated from the stomach as the endogenous ligand for growth hormone-secretagogue receptor (GHS-R). In addition to its unique role in regulating mealtime hunger and lipid metabolism, we have reported the physiological role of ghrelin in the regulation of insulin release and glucose metabolism. In this study, we uncovered that the signal transduction mechanisms of ghrelin in islet β-cells are very unique, being distinct from those utilized for growth hormone release. In type 2 diabetec GK rats, blockade of β-cell ghrelin receptor enhanced insulin release and prevents impaired glucose tolerance. Thus, manipulation of insulinostatic function of ghrelin?GHS-R system in islets could optimize the amount of insulin release to meet the systemic demand, providing a potential therapeutic application to prevent type 2 diabetes.
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