INFLUENCE OF ETHANOL ON THE LIVER METABOLISM OF FED AND STARVED RATS

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Abstract
The influence of ethanol on the metabolism of livers from fed and starved rats has been studied in liver-perfusion experiments. Results have been obtained on O2 consumption and CO2 production, on glucose release and uptake by the liver and on changes in the concentrations of lactate and pyruvate and of [beta]-hydroxybutyrate and acetoacetate in the perfusion medium. Oxygen consumption and CO2 production were lower in livers from starved rats than in livers from fed rats. Ethanol has no effect on the O2 consumption of either type of liver. After the addition of ethanol to the perfusion medium CO2 production ceased almost completely, the change being faster in livers from starved rats. With livers from fed rats glucose was released from the liver into the perfusion medium. This release was slightly greater when ethanol was present. With livers from starved rats no release of glucose was observed and when ethanol was added a marked uptake of glucose from the medium was found. A simultaneous release of glycolytic end products, lactate and pyruvate, into the medium occurred. Acetate was the main metabolite accumulating in the perfusion medium when ethanol was oxidized. With livers from starved rats a slightly increased formation of ketone bodies was found when ethanol was present. The lactate/pyruvate concentration ratio in the perfusion medium increased from 10 to 87 with livers from fed rats and from 20 to 171 with livers from starved rats when the livers were perfused with ethanol in the medium. The [beta]-hydroxybutyrate/ acetoacetate concentration ratio increased from 0.8 to 7.6 with livers from fed rats and from 1.0 to 9.5 with livers from starved rats when ethanol was added to the medium. The effects of ethanol are discussed and related to changes in the redox state of the liver that produce new conditions for some metabolic pathways.