| Project/Area Number |
23791017
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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 |
TAKAMOTO Iseki 東京大学, 医学部附属病院, 助教 (60431871)
|
|---|
| Research Collaborator |
窪田 直人
熊谷 勝義
中屋 恵三
小畑 淳史
門脇 孝
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
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)
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| Keywords | エネルギー / 糖質代謝異常 / 2型糖尿病 / 膵β細胞 / インスリン / Tcf7l2 |
|---|
| Research Abstract |
Common genetic variations of TCF7L2, one of the TCF/LEF transcription factors for the converging Wnt/β-catenin signaling pathway, are known to be associated with type 2 diabetes mellitus. To elucidate the role of TCF7L2-mediated pathway from the embryonic stage, genetically engineered mice were generated in which the dominant-negative form of Tcf7l2 expression was driven under the Rat Insulin Promoter. The phenotypes of theses mice suggest that the TCF7L2-mediated pathway in pancreatic β cells plays a crucial role in glucose metabolism through the regulation of β-cell mass and pancreatic insulin amount.
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