| Project/Area Number |
06671027
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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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 |
NOZAKI Shuichi Osaka Univ.Med School Ass.Prof., 医学部, 助手 (30252646)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Tadashi Osaka Univ.Med School Ass.Prof., 医学部, 助手 (90252668)
TAKEMURA Kaoru Osaka Univ.Med School Assoc.Prof., 医学部, 講師 (00161240)
MATSUZAWA Yuji Osaka Univ.Med School Prof., 医学部, 教授 (70116101)
平野 賢一 大阪大学, 医学部附属病院, 医員
毛受 正和 大阪大学, 医学部附属病院, 医員
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | hepatic lipase / remnant / HDL / atherosclerosis / リポフェクション |
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| Research Abstract |
In our previous reports, we clarified that the activity of hepatic lipase is inversely correlated with the levels of IDL-cholesterol in primary hyperlipidemic subjects and hypothyroidism, suggesting that hepatic lipase plays an important role on remnant metabolism. We further reported that low hepatic lipase activities were considered to be one of the major causes of high HDL cholesterol level in some type of hyperHDL-cholesterolemia We found that the dyslipidemia in primary biliary cirrhosis (PBC) is partly due to the low activity of hepatic lipase. In the present study, we report that the combined deficiency of hepatic and CETP is a risk for coronary artery disease in part due to reduced reverse cholesterol transport. These data suggested that increase of reverse cholesterol transport by hepatic lipase and CETP will facilitate cholesterol effulux from foam cell and prevent foam cell formation.In this study, based on these observations, we hyppothesized that the increase of hepatic lipase in vivo will decrease the extent of forming foam cells by increasing cholesterol reverse transport and decreasing the levels of remnant lipoproteins in plasma. We first made HVJ-liposome by incorpoating the gene with HVJ into liposome. The HVJ-liposome was injected into portal vein of rats and the expression of the gene in liver was investigated. We found that the expression in liver by the HVJ-liposome method was very low. We are now trying to establish the innovated method for the HVJ-liposome for establishing more highly expressing system in liver.
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