Analysis of intestinal lipid metabolism involved in the regulation for dietary lipid uptake.

最近，人们发现餐后血脂水平与心血管疾病的相关性比空腹水平更密切。然而，肠上皮细胞中脂肪酸氧化水平对餐后血脂的影响尚不清楚。本研究探讨了内源性和外源性调节脂类代谢的因素对餐后血脂的影响。因此，瘦素(一种内源性因子)和苯扎贝特(一种强大的PPAR-α激动剂)(一种外源性因子)通过促进肠道上皮细胞的脂肪酸氧化来抑制餐后血脂。特别是，在肥胖和糖尿病条件下以及生理条件下观察了PPAR-α激活的影响。此外，DHA，一种激活PPAR-α的食源性因子，也通过与苯扎贝特相同的机制抑制餐后血脂。这些结果表明，肠道上皮细胞的脂肪酸氧化是决定膳食脂肪摄取的一个重要因素。

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.