2015 Fiscal Year Final Research Report
Analysis of the mechanism of GCN2 activation in pancreatic beta cells
| Project/Area Number |
25461352
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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, 保健学研究科, 教授 (10335440)
|
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| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Keywords | 膵β細胞 / アミノ酸 / 2型糖尿病 |
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| Outline of Final Research Achievements |
We have previously clarified that GCN2 deficient mice displayed a reduced pancreatic beta cell mass. In this study, we aimed at elucidating the mechanism of the phenotype. As a result, GCN2 was found to regulate global translation by suppressing mTORC1 activity in beta cells when insulin translation was upregulated. This study showed that GCN2 inactivation or deficient resulted in pancreatic beta cell failure.
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| Free Research Field |
糖尿病学
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