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[β-内啡肽与肥胖症。可能的发病机制影响]

[Beta-endorphin and obesity. Possible pathogenetic implications].

作者信息

Giugliano D, Saccomanno F, Quatraro A, Ceriello A, Torella R

机构信息

I Facoltà di Medicina, Università degli Studi di Napoli, Cattedra di Diabetologia e Dietoterapia.

出版信息

Minerva Endocrinol. 1990 Apr-Jun;15(2):149-51.

PMID:2098658
Abstract

Several experimental data have documented the ability of both opiates and opioid peptides to stimulate food intake. On the other hand, the plasma beta-endorphin levels found in obese patients are higher than those observed in normal-weight controls, which may have pathogenetic implications. We have investigated the responses of plasma glucose, insulin, C-peptide and glucagon to an infusion of human beta-endorphin in formerly obese subjects who had obtained by dieting the normalization of body weight and in lean controls. The data show that: a) the increased plasma beta-endorphin concentrations found in human obesity are not corrected by normalization of body weight; b) formerly obese subjects behave as obese subjects in their metabolic and hormonal responses to beta-endorphin.

摘要

多项实验数据证明了阿片类药物和阿片肽均具有刺激食物摄入的能力。另一方面,肥胖患者体内的血浆β-内啡肽水平高于正常体重对照组,这可能具有致病意义。我们研究了曾肥胖但通过节食使体重恢复正常的受试者以及瘦对照组在输注人β-内啡肽后血浆葡萄糖、胰岛素、C肽和胰高血糖素的反应。数据显示:a)人类肥胖中发现的血浆β-内啡肽浓度升高不会因体重正常化而得到纠正;b)曾肥胖的受试者在对β-内啡肽的代谢和激素反应方面表现得与肥胖受试者一样。

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