| Project/Area Number |
20591081
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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 | Kagawa University |
|---|
Principal Investigator |
MURAO Koji Kagawa University, 医学部附属病院, 講師 (20291982)
|
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| Co-Investigator(Kenkyū-buntansha) |
IMACHI Hitomi 香川大学, 医学部・附属病院, 助教 (80380187)
ISHIDA Toshihiko 香川大学, 医学部, 教授 (50159737)
OHMORI Koji 香川大学, 医学部, 准教授 (00263913)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
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| Keywords | 脂質異常症 / 糖尿病 / HDL受容体 / SR-BI/CLA-1 / インクレチン / GLP-1 / ABCA1 / SR-BI / CLA-1 / チアゾリジン誘導体 / 高血糖 / p38-MAPK pathway / Sp1 / Fox01 / 血管内皮細胞 |
|---|
| Research Abstract |
Hyperglycemia suppressed the expression of HDL receptor SR-BI/CLA-1 via the activation of p38-MAPK pathway in Diabetes Mellitus. In diabetes mellitus, hyperglycemia stimulated atherosclerosis by inhibition of HDL metabolism. On the other hand, TZD stimulated the expression of SR-BI/CLA-1 in liver via the activation of PPARs.
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