| Project/Area Number |
09557079
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
内分泌・代謝学
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| Research Institution | University of Tokyo |
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Principal Investigator |
YAMADA Nobuhiro University of Tokyo, Faculty of Medicine, Associate Prof., 医学部・附属病院, 助教授 (40200729)
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| Co-Investigator(Kenkyū-buntansha) |
YAHAGI Naoya University of Tokyo, Faculty of Medicine, Research Fellow, 医学部・附属病院, 医員
HARADA Kenji University of Tokyo, Faculty of Medicine, Research Fellow, 医学部・附属病院, 医員
ISHIBASHI Shun University of Tokyo, Faculty of Medicine, Research Associate, 医学部・附属病院, 助手 (90212919)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 1998: ¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 1997: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | atherosclerosis / obesity / hormone-sensitive lipase / knockout mouse |
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| Research Abstract |
We intend to study the mechanism of lipid accumulation in arterial wall and fat tissue by studying intracellular lipid metabolism, to clarify the common pathophysiology of atherosclerosis, obesity, hyperlipidemia, and glucose tolerance. As a candidate of insulin-sensitive gene concerning the lipid accumulation which is commonly observed in arteriosclerosis, obesity, and hyperlipidemia, we paid attention to hormone sensitive lipase(HSL)and neutral cholesterol ester hydrolase(NCEH)which may be identical in the regulation of intracellular cholesterol metabolism and triglyceride metabolim. In this study, we try to clarify the common mechanism for atherosclerosis and obesity by gene targeting of HSL.
We had already succeeded in gene targeting of HSL, and the series of the HSL knockout mouse was established. The male infertility was recognized when the phenotype of the HSL knockout mouse was analyzed. It was indicated that HSL was related to the spermatogenesis. The obvious lowering of plasma FFA level was not recognized, though the blood FFA level decreased, indicating that novel neutral fat degrading enzyme except for HSL exists in fat tissue. The pathophysiology of obesity, insulin resistance, and glucose tolerance in this mouse model will be examined.
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