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饮食中碳水化合物和乙醇引起的化学物质代谢及毒性改变。

Dietary carbohydrate-and ethanol-induced alteration of the metabolism and toxicity of chemical substances.

作者信息

Sato A, Nakajima T

出版信息

Nutr Cancer. 1984;6(2):121-32.

PMID:6400176
Abstract

This paper is a review of experimental data leading to three main conclusions: Food deprivation causes a 2- to 3-fold increase in the metabolism of various chemicals in rat liver, such as chloroform and carbon tetrachloride. The lack of carbohydrate rather than the lack of protein or fat accompanying food deprivation is primarily responsible for the increase. In contrast to general belief, dietary carbohydrate plays an important role in regulating drug-metabolizing enzyme activity in the liver: a low-carbohydrate diet enhances, whereas a high-carbohydrate diet represses, the hepatic metabolism of a variety of volatile hydrocarbons, irrespective of protein and/or fat content(s). Ethanol and carbohydrate are antagonistic in connection with hepatic metabolism: the former increases and the latter decreases it. A decrease (increase) in carbohydrate intake augments (suppresses) the action of ethanol in a dose-related manner: ethanol consumed with lowered carbohydrate intake results in a more remarkable increase in hepatic metabolism than does ethanol consumed with moderate carbohydrate intake. Further study should be conducted to determine whether the conclusions reached also apply to the metabolism of foreign chemicals other than volatile hydrocarbons.

摘要

本文是对实验数据的综述,得出了三个主要结论:食物剥夺会使大鼠肝脏中多种化学物质(如氯仿和四氯化碳)的代谢增加2至3倍。食物剥夺时伴随的碳水化合物缺乏而非蛋白质或脂肪缺乏是导致这种增加的主要原因。与普遍看法相反,膳食碳水化合物在调节肝脏药物代谢酶活性方面起着重要作用:低碳水化合物饮食会增强,而高碳水化合物饮食会抑制多种挥发性碳氢化合物的肝脏代谢,无论蛋白质和/或脂肪含量如何。乙醇和碳水化合物在肝脏代谢方面具有拮抗作用:前者增加而后者降低肝脏代谢。碳水化合物摄入量的减少(增加)会以剂量相关的方式增强(抑制)乙醇的作用:与中等碳水化合物摄入量时摄入的乙醇相比,碳水化合物摄入量降低时摄入的乙醇会导致肝脏代谢更显著的增加。应进一步开展研究,以确定所得出的结论是否也适用于挥发性碳氢化合物以外的外来化学物质的代谢。

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