Abstract

Certain fractions of brain homogenate prepared from ethanol-treated rats consumed glucose and produced lactate at increased rates. These effects of ethanol were even larger when glucose-6-phosphate was used as substrate, but smaller with glucose-1-phosphate. Measurement of the utilization of U-[ 14C]glucose in a system designed for the assay of hexokinase showed that the formation of acidic metabolites was also augmented as a result of ethanol treatment. By contrast, when ethanol was added in vitro in corresponding concentrations, the catabolism of glucose decreased. Data are presented on the effects of varied conditions during incubation, of the use of homogenates from other tissues, of the interval from administration of ethanol to killing, and of the amount of ethanol administered. The concentration of γ-aminobutyric acid during incubation with glutamic acid increased with increasing concentration of glucose in the medium, while the concentrations of glutamine and aspartic acid decreased. The concentrations of γ-aminobutyric acid and glutamine increased continuously as functions of time, but the concentration of aspartic acid was maximal at an early phase of incubation. It is concluded that under the influence of ethanol the brain utilizes increased amounts of glucose, while the catabolism of γ-aminobutyric acid and glutamic acid as well as the formation of glutamine decrease.

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