Angptl4 作为内源性肠脂质消化抑制剂。
Angptl4 serves as an endogenous inhibitor of intestinal lipid digestion.
机构信息
Nutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen University, Bomenweg 2, 6703 HD Wageningen, The Netherlands.
Human and Animal Physiology, Department of Animal Sciences, Wageningen University, 6700 EV Wageningen, The Netherlands.
出版信息
Mol Metab. 2013 Nov 20;3(2):135-44. doi: 10.1016/j.molmet.2013.11.004. eCollection 2014 Apr.
Dietary triglycerides are hydrolyzed in the small intestine principally by pancreatic lipase. Following uptake by enterocytes and secretion as chylomicrons, dietary lipids are cleared from the bloodstream via lipoprotein lipase. Whereas lipoprotein lipase is inhibited by several proteins including Angiopoietin-like 4 (Angptl4), no endogenous regulator of pancreatic lipase has yet been identified. Here we present evidence that Angptl4 is an endogenous inhibitor of dietary lipid digestion. Angptl4-/- mice were heavier compared to their wild-type counterparts without any difference in food intake, energy expenditure or locomotor activity. However, Angptl4-/- mice showed decreased lipid content in the stools and increased accumulation of dietary triglycerides in the small intestine, which coincided with elevated luminal lipase activity in Angptl4-/- mice. Furthermore, recombinant Angptl4 reduced the activity of pancreatic lipase as well as the lipase activity in human ileostomy output. In conclusion, our data suggest that Angptl4 is an endogenous inhibitor of intestinal lipase activity.
饮食中的甘油三酯主要在小肠中被胰腺脂肪酶水解。在肠细胞摄取并分泌为乳糜微粒后，脂蛋白脂肪酶将膳食脂质从血液中清除。尽管脂蛋白脂肪酶受到包括血管生成素样蛋白 4（Angptl4）在内的多种蛋白质的抑制，但尚未鉴定出胰腺脂肪酶的内源性调节剂。本文作者提供的证据表明，Angptl4 是饮食脂质消化的内源性抑制剂。与野生型相比，Angptl4-/- 小鼠的体重更重，但食物摄入量、能量消耗或运动活性没有差异。然而，Angptl4-/- 小鼠的粪便脂质含量减少，小肠中膳食甘油三酯的积累增加，这与 Angptl4-/- 小鼠肠腔内脂肪酶活性升高相一致。此外，重组 Angptl4 降低了胰腺脂肪酶以及人回肠造口术输出物中的脂肪酶活性。总之，本文数据表明，Angptl4 是肠道脂肪酶活性的内源性抑制剂。
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