A model has been developed for the administration to the baboon of ethanol as part of a nutritionally adequate liquid diet. With this regimen, all animals maintained their weight, and liver morphology was normal in the controls. Isocaloric substitution of carbohydrate (50% of total calories) by ethanol resulted in the production of fatty liver in all animals, while some also developed alcoholic hepatitis and cirrhosis with increased activities of serum glutamic oxaloacetic transaminase. Inebriation and manifestation of dependence upon withdrawal of the diet were observed. Chemical alterations produced by ethanol at the fatty liver stage were characterized by striking triglyceride accumulation and enhanced activities of microsomal enzymes, including the microsomal ethanol oxidizing system (MEOS).

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