Investigation of unknown mechanism of glucose metabolism regulated by cell cycle control related protein p21.
| Project/Area Number |
24790912
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KUBOTA Midori 東京大学, 保健・健康推進本部, 助教 (20383804)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 細胞周期 / インスリン抵抗性 / p21 |
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| Outline of Final Research Achievements |
p21 is the main factor which controls cell cycle and accelerated in hepatocyte and adipocyte of obese model mice, but though cell cycle of those cells is G0 periods.
Previous research has shown that overexpression of p21 decrease insulin-stimulated glucose uptake in 3T3-L1 cultured adipocytes and p21 knockout mice fed high fat diet has reduced insulin resistance. CDKs (cyclin-dependent kinases) is known as a target molecule of p21. So when several CDK inhibitors were treated in 3T3-L1 adipocytes, insulin-stimulated glucose uptake was decreased.
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Report
(4 results)
Research Products
(2 results)
