1985Nutrition and CancerRequires access

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

Akio Sato, Tamie Nakajima

Open publisher page 19 citations

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.

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What this paper is about

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.

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Available 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.

Key concepts: Carbohydrate, Carbohydrate metabolism, Ethanol, Metabolism, Chemistry, Toxicity, Carbon tetrachloride, Drug metabolism

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