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酒精对脂蛋白代谢的影响。I. 高密度脂蛋白结合

Effect of alcohol on lipoprotein metabolism. I. High density lipoprotein binding.

作者信息

Parkes J G, Hussain R A, Goldberg D M

机构信息

Department of Clinical Biochemistry, Banting Institute, University of Toronto, Ont., Canada.

出版信息

Clin Physiol Biochem. 1989;7(6):269-77.

PMID:2560688
Abstract

The effects of ethanol upon the binding of [125I]-labelled human high density lipoprotein 3 (HDL3) was examined in rat liver microsomes and monolayer cultures of human hepatoma (Hep G2) cells. Alcohol feeding to rats (35% caloric content) caused a significant (p less than 0.05) increase in serum cholesterol concentrations relative to pair-fed controls, but HDL3 binding to rat liver microsomes was unaffected by alcohol consumption. By contrast, addition of 10 mM ethanol to Hep G2 cells increased HDL3 binding, and this increase was observed after 14, 28 and 40 days of exposure. This alcohol-dependent rise in HDL3 binding was associated with a 2.3- to 5-fold rise in receptor number (Bmax), and a 2- to 6-fold increase in the dissociation constant (Kd). The data suggest that the net effect of increased receptor number and lower receptor affinity is to increase the capacity of hepatocytes to metabolize circulating high density lipoproteins, and that this increase in the face of elevated plasma high density lipoprotein cholesterol consequent upon alcohol consumption would facilitate greater mobilization of cholesterol from peripheral tissues to the liver.

摘要

在大鼠肝微粒体和人肝癌(Hep G2)细胞单层培养物中研究了乙醇对[125I]标记的人高密度脂蛋白3(HDL3)结合的影响。给大鼠喂食含35%热量的酒精,与配对喂食的对照组相比,血清胆固醇浓度显著(p<0.05)升高,但HDL3与大鼠肝微粒体的结合不受酒精摄入的影响。相比之下,向Hep G2细胞中添加10 mM乙醇可增加HDL3的结合,并且在暴露14、28和40天后均观察到这种增加。HDL3结合的这种酒精依赖性升高与受体数量(Bmax)增加2.3至5倍以及解离常数(Kd)增加2至6倍有关。数据表明,受体数量增加和受体亲和力降低的净效应是增加肝细胞代谢循环中高密度脂蛋白的能力,并且在饮酒后血浆高密度脂蛋白胆固醇升高的情况下,这种增加将有助于将更多胆固醇从外周组织转运至肝脏。

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引用本文的文献

1
Long-term ethanol consumption impairs reverse cholesterol transport function of high-density lipoproteins by depleting high-density lipoprotein sphingomyelin both in rats and in humans.长期饮酒会通过消耗大鼠和人类体内的高密度脂蛋白鞘磷脂,损害高密度脂蛋白的逆向胆固醇转运功能。
Metabolism. 2007 Jul;56(7):947-53. doi: 10.1016/j.metabol.2007.03.003.