| Project/Area Number |
12671127
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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 | TEIKYO UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
MAKOTO Kinoshita TEIKYO UNIVERSITY SCHOOL OF MEDICINE, ASSOCIATE PROFESSOR, 医学部, 助教授 (70186295)
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| Co-Investigator(Kenkyū-buntansha) |
KAZUHISA Tsukamoto DEPARTMENT OF MEDICINE, TOKYO UNIVERSITY, ASSISTANT PROFESSOR, 医学部, 助手 (20251233)
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| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | SR-B1 / bile acid / resin / HDL / 受容体 |
|---|
| Research Abstract |
Scanenger receptor type B1 (SR-B1) is an unique receptor of HDL which uptake cholesteryl ester from HDL. Therefore, mouse which overexpress SR-B1 mRNA showed low HDL cholesterol concentration. In despite of low HDL cholesterol concentration, mouse which overexpress SR-B1 mRNA showed resistance against atherosclerotic formula diet.
In our study, it was revealed that SR-B1 remodulate the large HDL that were observed in CETP deficient patient into normal HDL particle. And the expression of SR-B1 mRNA of liver was increased according to the amount of bile acid secretion. It may be concluded that SR-B1 may change the atherogenic large HDL into normal anti-atherogenic HDL.
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