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全胃肠外营养对人体低密度脂蛋白分解代谢的促进作用。

Acceleration of low-density lipoprotein catabolism in man by total parenteral nutrition.

作者信息

Chait A, Foster D, Miller D G, Bierman E L

出版信息

Proc Soc Exp Biol Med. 1981 Oct;168(1):97-104. doi: 10.3181/00379727-168-41240.

DOI:10.3181/00379727-168-41240
PMID:6798574
Abstract

Since insulin enhances the catabolism of low-density lipoprotein (LDL) by cultured human cells, a potential role of insulin in the regulation of plasma LDL levels in man is suggested. To evaluate the possible effect of insulin on LDL catabolism in vivo, the disappearance rates of injected 125I-labeled autologous LDL were determined before and after endogenous hyperinsulinemia was evoked by total parenteral nutrition. Multicompartmental analysis of plasma decay curves showed a 26% increase in the fractional catabolic rate of LDL after total parenteral nutrition was started. An associated reduction of plasma cholesterol levels resulted from changes in both LDl and high-density lipoprotein. These results suggest that the reduction of LDL levels during total parenteral nutrition is at least partly accounted for by enhanced LDL catabolism. It is postulated that the enhanced LDL catabolism may result from the hyperinsulinemia that accompanies total parenteral nutrition, via insulin stimulation of receptor-mediated LDL catabolism.

摘要

由于胰岛素可增强培养的人体细胞对低密度脂蛋白(LDL)的分解代谢,提示胰岛素在调节人体血浆LDL水平中可能发挥作用。为评估胰岛素在体内对LDL分解代谢的可能影响,在通过全胃肠外营养诱发内源性高胰岛素血症前后,测定了注射的125I标记自体LDL的消失率。血浆衰变曲线的多室分析显示,开始全胃肠外营养后,LDL的分解代谢率分数增加了26%。LDL和高密度脂蛋白的变化导致血浆胆固醇水平相应降低。这些结果表明,全胃肠外营养期间LDL水平的降低至少部分是由于LDL分解代谢增强所致。据推测,LDL分解代谢增强可能是由于全胃肠外营养伴随的高胰岛素血症,通过胰岛素刺激受体介导的LDL分解代谢所致。

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