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载脂蛋白A-IV在食物摄入调节中的作用。

The role of apolipoprotein A-IV in the regulation of food intake.

作者信息

Tso P, Liu M, Kalogeris T J, Thomson A B

机构信息

Department of Pathology, University of Cincinnati, Cincinnati, Ohio 45267, USA.

出版信息

Annu Rev Nutr. 2001;21:231-54. doi: 10.1146/annurev.nutr.21.1.231.

DOI:10.1146/annurev.nutr.21.1.231
PMID:11375436
Abstract

Apolipoprotein A-IV (apo A-IV) is a glycoprotein synthesized by the human intestine. In rodents, both the small intestine and liver secrete apo A-IV, but the small intestine is the major organ responsible for the circulating apo A-IV. Intestinal apo A-IV synthesis is markedly stimulated by fat absorption and appears not to be mediated by the uptake or reesterification of fatty acids to form triglycerides. Rather, the formation of chylomicrons acts as a signal for the induction of intestinal apo A-IV synthesis. Intestinal apo A-IV synthesis is also enhanced by a factor from the ileum, probably peptide tyrosine-tyrosine. The inhibition of food intake by apo A-IV is mediated centrally. The stimulation of intestinal synthesis and the secretion of apo A-IV by lipid absorption are rapid; thus, apo A-IV likely plays a role in the short-term regulation of food intake. Other evidence suggests that apo A-IV may also be involved in the long-term regulation of food intake and body weight. Chronic ingestion of a high-fat diet blunts the intestinal apo A-IV response to lipid feeding and may explain why the chronic ingestion of a high-fat diet predisposes both animals and humans to obesity.

摘要

载脂蛋白A-IV(apo A-IV)是一种由人体肠道合成的糖蛋白。在啮齿动物中,小肠和肝脏都会分泌apo A-IV,但小肠是循环中apo A-IV的主要来源器官。脂肪吸收可显著刺激肠道apo A-IV的合成,且这一过程似乎并非由脂肪酸摄取或再酯化形成甘油三酯介导。相反,乳糜微粒的形成充当了诱导肠道apo A-IV合成的信号。来自回肠的一种因子(可能是肽酪氨酰酪氨酸)也可增强肠道apo A-IV的合成。apo A-IV对食物摄入的抑制作用是通过中枢介导的。脂质吸收对肠道apo A-IV合成和分泌的刺激作用迅速;因此,apo A-IV可能在食物摄入的短期调节中发挥作用。其他证据表明,apo A-IV也可能参与食物摄入和体重的长期调节。长期摄入高脂饮食会减弱肠道对脂质喂养的apo A-IV反应,这可能解释了为什么长期摄入高脂饮食会使动物和人类都易患肥胖症。

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