| Project/Area Number |
60480268
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | Osaka University |
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Principal Investigator |
YUJI Matsuzawa Summarization, Investigation of lipid transfer between each lipoprotein, 医学部, 助手 (70116101)
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| Co-Investigator(Kenkyū-buntansha) |
SHIZUYA Yamashita Cell culture and investigation of lipoprotein receptors, 医学部附属病院, 医員 (60243242)
KAORU Kameda Clinical studies on the cases with hyper- <HDL_2> -cholesterolemia, 医学部, 助手 (00161240)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1986: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1985: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | HDL-cholesterol / corneal opacification / coronary heart disease / reverse cholesterol transport / 角膜混濁 / 動脈硬化コレステロールエステル転送活性 / CE転送蛋白 / LDL受容体 / 家族性高コレステロール血症 |
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| Research Abstract |
1. We found peculiar cases with familial hyperalphalipoproteinemia who have the symptoms of lipid storage such as premature corneal opacification or coronary heart disease in spite of markedly high levels of HDL-cholesterol (140-160 mg/dl). The serum levels of apolipoprotein A-I and E in these cases were also elevated. Ultracentrifugation analysis disclosed that the excess levels of HDL-cholesterol were mainly due to increases in cholesteryl ester (CE) in <HDL_2> fraction. The activity of hepatic triglyceride lipase was very low in both patients. The net transfer of cholesteryl ester was present, but it occurred from VLDL and LDL to HDL, in the opposite direction to normal control leading to the accumulation of CE in HDL. These abnormal cholesteryl ester transfer should be involved in the pathogenesis of cholesterol accumulation in <HDL_2> leading to the impairment of the reverse cholesterol transfer through HDL and to the lipid storage in the tissues.
In addition to these cases, we also found three cases with familial hyper- <HDL_2> -cholesterolemia caused by the deficiency of CE transfer protein. These cases showed no symptoms of lipid storage. From these studies the role of HDL in lipoprotein metabolism, especially in cholesterol transport, will be elucidated.
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