Molecular mechanism for the phenotypic expression of metabolic syndrome. -CD36 deficiency as a model-
Project/Area Number |
16590882
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Metabolomics
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Research Institution | OSAKA UNIVERSITY |
Principal Investigator |
HIRANO Ken-ichi Osaka University, Graduate School of Medicine, Assistant, 医学系研究科, 助手 (30332737)
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Project Period (FY) |
2004 – 2005
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Project Status |
Completed (Fiscal Year 2005)
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Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
|
Keywords | Metabolic syndrome / CD36 / Postprandial hyperlipidemia / HDL / 代謝異常 / 動脈硬化 / 脂肪酸 |
Research Abstract |
Human CD36 deficiency is a monogenic form of metabolic syndrome expressing dyslipidemia at both fasting and postprandial states. The aim of the present study was to investigate molecular mechanism underlying postprandial hypertriglyceridemia using CD36 knockout mice as a model. Oral fat loading test exhibited postprandial increase of triglycerides in CD36 null mice, which was similar to those observed in human CD36 deficiency. The combination experiments with oral fat loading and the injection of triton WR 1339,which inhibits lipolysis of lipoproteins, suggested an accelerated intestinal secretion of lipoproteins. In order to ascertain the above data, we analyzed lipids and lipoproteins of intestinal lymph fluid by puncturing cisterna chili after oral fat loading, indicating higher TG levels of in lymph fluid of CD36 null mice. Furthermore, the histological analyses demonstrated that oil droplets were observed much abundant in the earlier phase of oral fat loading. These results suggested that the accelerated fat absorption from intestines is one of the major causes of postprandial hypertriglyceridemia in CD36 deficiency.
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Report
(3 results)
Research Products
(19 results)
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[Journal Article] Defective cholesterol efflux in Werner syndrome fibroblasts and its phenotypic correction by Cdc42, a RhoGTPase.2005
Author(s)
Zhang Z, Hirano K, Tsukamoto K, Ikegami C, Koseki M, Saijo K, Ohno T, Sakai N, Hiraoka H, Shimomura I, Yamashita S.
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Journal Title
Exp Geront. 40
Pages: 286-294
Description
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