| Project/Area Number |
20591051
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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 | The University of Tokyo |
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Principal Investigator |
OHSUGI Mitsuru The University of Tokyo, 医学部附属病院, 助教 (00420216)
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| Co-Investigator(Renkei-kenkyūsha) |
KADOWAKI Takashi 東京大学, 医学部附属病院, 教授 (30185889)
UEKI Kohjiro 東京大学, 医学部附属病院, 准教授 (00396714)
KUBOTA Naoto 東京大学, 医学部附属病院, 特任 (50396719)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 膵β細胞 / IRS / CREB / CaMK / 糖尿病 / 代償性肥大 / lRS-2 / カルモジュリン依存性キナーゼ |
|---|
| Research Abstract |
(1) High glucose levels or glucose stimulation predominantly control pancreatic β cell IRS-2 levels. (2) A transcription factor CREB is critical for regulating β cell IRS-2 expression levels. Calmodulin dependent kinase 4 is stimulated by glucose, and the kinase appears to be the key component of complex regulation of CREB activation in pancreatic β cells. (3) In models of pancreatic β cell failure, such as db/db mice, critical molecules of glucose sensing, including glucokinase and glucose transporter 2, are downregulated, thus leading to a net decrease in glucose flux to β cells. With resultant reduction in IRS-2 levels, pancreatic β cell lose a key component of adaptive β cell proliferation and survival.
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