| Project/Area Number |
23791048
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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 | Osaka University (2012)
独立行政法人医薬基盤研究所 (2011) |
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Principal Investigator |
UEBI Tastuya 大阪大学, 大学院・生命機能研究科, 招へい研究員 (80513803)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | メタボリックシンドローム / 肥満 / 脂質代謝 / リン酸化 / コレステロール代謝 |
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| Research Abstract |
SIK3-KO mice do not get fat, but were caused liver dysfunction. In order to develop the anti-obesity drug, in this study, a function of SIK3 was analyzed. SIK3-KO mice were high sensitive to bile acid, and the high bile acid level induced serious liver dysfunction. By analysis of gene expression level, it was found that SIK-KO mice lost the regulation of expression of gene related to cholesterol and bile acid responding a diet.It was suggested that SIK3 was master regulator of cholesterol and bile acid homeostasis. By mass spectrometry analysis of phosphorylatedproteins, two candidate target proteins of SIK3 were found. Since there was no difference in the fatty acid composition between SIK3-KO and wild type, it was suggested that fatty acid do not relate to energy reflux.
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