| Project/Area Number |
24659443
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OKAZAKI Hiroaki 東京大学, 医学部附属病院, 特任准教授 (80610211)
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| Co-Investigator(Renkei-kenkyūsha) |
TAKANASHI Mikio 東京大学, 医学部附属病院, 特任助教 (70610799)
TAKAMOTO Iseki 東京大学, 医学部附属病院, 特任助教 (60431871)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 糖尿病 / 脂質 / インスリン分泌 / 脂肪細胞 / リパーゼ / メタボローム解析 / インスリン / 脂肪分解 / インスリン分泌刺激物質 |
|---|
| Research Abstract |
This study was aimed at elucidating the molecular mechanisms of catecholamine-induced insulin secretion. We have previously identified a profound defect of this phenomenon in mice with a targeted disruption of HSL, which is one of the major lipases involved in adipocyte lipolysis. As the plasma levels of hormones that affect insulin secretion were similar between wild-type and HSLKO mice, we reasoned some lipolytic products of HSL in adipocytes stimulate insulin secretion from beta cells in pancreas. Through metabolomics approach, we have identified several candidates, which have been further tested for the ability to stimulate insulin secretion.
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