| Project/Area Number |
22380075
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Food science
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KAWADA Teruo 京都大学, 大学院・農学研究科, 教授 (10177701)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2012: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2011: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2010: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | 食品機能 / メタボリックシンドローム / 腸管上皮細胞 / 脂肪酸酸化 / 脂質異常症 / 食後高脂血症 / PPAR / 小腸上皮細胞 / 食品成分 / 生活習慣病 |
|---|
| Research Abstract |
Recently, postprandial serum lipid levels have been found to correlate more closely to cardiovascular diseases than fasting levels. However, the effect of fatty acid oxidation levels in intestinal epithelial cells on postprandial lipidemia ha s not been clarified. In this study, the effects of endogenous and exogenous factors involved in the regulation of lipid metabolism on postprandial lipidemia were examined. As a result, leptin (an endogenous factor) and bezafibrate, a potent PPAR-alpha agonist, (an exogenous one) suppressed postprandial lipidemia through enhancing fatty acid oxidation in intestinal epithelial cells. Particularly, the effects of PPAR-alpha activation were observed under obese and diabetic conditions as well as physiological conditions. Moreover, DHA, a food-derived factor activating PPAR-alpha, also suppressed postprandial lipidemia through the same mechanism of bezafibrate. These results suggest that the fatty acid oxidation in intestinal epithelial cells is an important factor determining dietary lipid uptake.
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