Enterostatin--a peptide regulating fat intake.
Enterostatin--a peptide regulating fat intake.
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肠抑素——一种调节脂肪摄入的肽。
DOI：
10.1002/j.1550-8528.1997.tb00565.x
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
York,D
中科院分区：
文献类型：
--
作者：
Erlanson-Albertsson,C;York,D
Erlanson-Albertsson，Charlotte，David York.肠抑素-一种调节脂肪摄入量的多肽。高脂肪摄入量，以及无法将脂肪氧化与脂肪摄入量相匹配，已被发现与人类肥胖有关。这篇综述描述了我们目前对肠抑素的理解，肠抑素是一种选择性地减少脂肪摄入量的多肽。肠抑素是由分泌的胰腺前脂肪酶在肠道中裂解形成的，剩余的脂肪酶在脂肪消化过程中是胰腺脂肪酶必不可少的辅助因子。肠抑素也在胃粘膜和小肠粘膜上皮细胞中产生。高脂饮食增加了原脂肪酶基因转录和肠抑素释放到胃肠管腔。喂食后，肠抑素出现在淋巴和循环中。在正常喂养和涉及饮食选择的实验范例中，Enterostatin将选择性地抑制脂肪摄取。它的厌食作用已在许多物种中得到证实。已经提出了外围和中心两个行动地点。外周机制涉及到下丘脑中枢的迷走神经传入信号通路。中枢反应通过一条既包括5-羟色胺能成分又包括阿片能成分的通路进行调节。从长期来看，肠抑素可以减少脂肪摄入量、体重和体脂。这种反应可能涉及肠抑素的多种代谢效应，包括减少胰岛素分泌，增加对棕色脂肪组织的交感冲动，以及刺激肾上腺皮质类固醇的分泌。研究表明，肥胖和偏爱饮食脂肪的大鼠品系的肠抑素产量和/或反应性较低，这可能是一种病理生理学作用。与正常体重的人相比，肥胖的人在一顿试餐后也表现出较低的胰腺前脂肪酶分泌。
ERLANSON‐ALBERTSSON, CHARLOTTE, DAVID YORK. Enterostatin‐a peptide regulating fat intake.A high fat intake, together with an inability to match lipid oxidation to fat intake, has been found to be correlated with obesity in humans. This review describes our current understanding of enterostatin, a peptide that selectively reduces fat intake. Enterostatin is formed in the intestine by the cleavage of secreted pancreatic procolipase, the remaining colipase serving as an obligatory cofactor for pancreatic lipase during fat digestion. Enterostatin is also produced in the gastric mucosa and the mucosal epithelia of the small intestine. Procolipase gene transcription and enterostatin release into the gastrointestinal lumen are increased by high‐fat diets. After feeding, enterostatin appears in the lymph and circulation. Enterostatin will selectively inhibit fat intake during normal feeding and in experimental paradigms that involve dietary choice. Its anorectic effect has been demonstrated in a number of species. Both peripheral and central sites of action have been proposed. The peripheral mechanism involves an afferent vagal signaling pathway to hypothalamic centers. The central responses are mediated through a pathway that includes both serotonergic and opioidergic components. Chronically, enterostatin reduces fat intake, bodyweight, and body fat. This response may involve multiple metabolic effects of enterostatin, which include a reduction of insulin secretion, an increase in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. A possible pathophysiological role is suggested by studies that have linked low enterostatin production and/or responsiveness to strains of rat that become obese and prefer dietary fat. Humans with obesity also exhibit a lower secretion of pancreatic procolipase after a test meal, compared with persons of normal weight.