Modification of Metabolic Effects of Ethanol by Fructose

Present knowledge of the metabolic interactions between fructose and ethanol in man and laboratory animals is reviewed. The possible biochemical mechanisms of these interactions are considered. Some new data on the effects of fructose and ethanol on carbohydrate and lipid metabolism are included. Fructose increases the effects of ethanol on the hepatic lactate/pyruvate and a ‐glycerophosphate/dihydroxyacetone phosphate ratios. Thus it augments the basic metabolic effect of ethanol, i.e. reduction of the hepatic redox state. The ethanol‐induced increase in hepatic a ‐glycerophosphate concentration has been regarded as an important factor in the pathogenesis of the acute alcoholic fatty liver. But although fructose causes hypertriglyceridaemia and augments the effect of ethanol on hepatic a ‐glycerophosphate concentration, it was found to diminish the ethanol‐induced accumulation of triglycerides in the liver. Glucose had a similar effect. The reason for this is uncertain, but the inhibition of peripheral lipolysis by fructose and glucose might be partly responsible. The most important effect of ethanol on carbohydrate metabolism is to inhibit hepatic gluconeogenesis by producing NADH in excess. Although the production of glucose from fructose is not directly dependent on the redox state of the liver, it is slightly inhibited by ethanol in vitro. However, in vivo fructose is effectively converted to glucose even during ethanol oxidation, and in ethanol‐induced hypoglycaemia it rapidly restores the blood glucose level.