| Budget Amount *help |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2010: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2009: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2008: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Research Abstract |
High density lipoproteins (HDL) are known to prevent from development of atherosclerosis and the reduction of HDL is one of the risk factors for coronary heart disease. HDL and their component, apolipoprotein (Apo) A-I, take up cholesterol from atherosclerotic plaques and transport it back to the liver, a system called "reverse cholesterol transport (RCT)". Both ApoA-I and ATP-binding cassette transporter A1 (ABCA1) are the rate-limiting factors that generate HDL in the liver. We for the first time identified adiponectin (APN) from adipocytes that inhibits the development of atherosclerosis. We found a positive correlation between plasma high density lipoprotein-cholesterol (HDL-C) and APN concentrations in humans. We have shown that APN accelerates RCT by increasing the hepatic expression of ApoA-I and ABCA1, using HepG2 cells. In contrast, APN reduced the expression of ApoB100 mRNA and secretion of ApoB100 into the medium. We elucidated the importance of COUP-TF2, one of the nuclear receptors, a new regulator of lipoprotein metabolism, that may prevent atherosclerosis by increasing HDL synthesis by enhancing ApoA-I and ABCA1 and by reducing ApoB100 (VLDL) secretion.
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