Nutritional factors required for alcoholic liver disease in rats

Decades ago it was suggested that nutritional factors are important in the development of alcoholic liver disease (ALD). However, several models of experimental alcoholism considered that the diets fed to animals were nutritionally adequate, complete and balanced. Therefore, a concept prevailed that the effects observed were due to alcohol per se and that they occurred despite a nutritionally adequate status in the animal. Examination of various models revealed that animals were malnourished because they ingested reduced levels of macro- and micronutrients. Furthermore, they consumed only small amounts of carbohydrate and a high level of unsaturated fat for long periods during the development of ALD. Alcoholic rats show many effects of inadequate nutritional status, such as a slow growth, depressed levels of liver glycogen and pancreatic amylase, enhanced protein degradation and circulating levels of branched-chain amino acids, and increased levels of enzymes involved in gluconeogenesis and alterations in the activities of enzymes related to the metabolism of carbohydrate as compared with controls. Chronic consumption of alcohol did not result in fatty liver, high blood alcohol concentration (BAC) or other observed effects when intake of energy, carbohydrate and other nutrients was increased. Furthermore, pre-existing effects of alcohol consumption, such as fatty liver, BAC and delayed gastric emptying, were reversed in rats receiving increased energy and carbohydrate intakes while continuing alcohol ingestion. Thus, nutritional status of the animal determines the production or prevention of ALD or other effects that were considered to be due to alcohol alone.