| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Research Abstract |
Increased secretion of apolipoprotein B (apoB)-containing lipoproteins, particularly VLDL, and hepatic steatosis are characteristic concomitants of insulin resistance, the metabolic syndrome, and type 2 diabetes. Endoplasmic reticulum (ER) stress plays a central role in the development of hepatic insulin resistance and steatosis. Each fattyacid (FA), when administered for prolonged periods of time, can, at certain doses, inhibit apoB secretion. The effects of OA and PA parallel their ability to induce ER stress; PA is more potent and acts, in part, via ceramide. DHA is the most potent inhibitor but this is independent of ER stress.
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