GCN2, a type 2 diabetes mellitus susceptibility gene,is associated with the regulation of pancreatic beta-cell mass
| Project/Area Number |
22590981
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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 | Kobe University |
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Principal Investigator |
KIDO Yoshiaki 神戸大学, 大学院・保健学研究科, 教授 (10335440)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | エネルギー / 糖質代謝異常 / 糖尿病 / 膵β細胞 / GCN2 / インスリンシグナル / 膵β細胞量 |
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| Research Abstract |
GCN2 is a molecule activated by amino acid deficiency. We generated generalized GCN2 knockout mice (GCN2-/- mice). GCN2-/- mice fed a high-fat diet (HFD) exhibited significant aggravation in glucose tolerance and reduction in pancreatic ・-cell mass. Our results showed that chronic activation of mTORC1 signal is one of the causes of reduction in pancreatic ・-cell mass in GCN2-/- mice. In islets from mice fed a HFD, the activation of GCN2, caused by the enhancement of translation of insulin, might contribute to maintenance of pancreatic ・-cell mass.
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Report
(4 results)
Research Products
(10 results)
