Pathology of Choline Deficiency
Some 50 years ago Best et al. (1) reported that fatty degeneration of the liver in diabetic dogs kept on a lean meat and sugar diet could be alleviated by the administration of lecithin. The observation led these investigators to identify the lipotropic action of choline, a component of lecithin (2). The term lipotropic was applied to dietary substances that either prevent the deposition of abnormal amounts of lipids in the liver or accelerate their removal into the circulation (3,4). Within a relatively short time thereafter, the importance of choline, in addition to its lipotropic action, was recognized in the general nutritional requirement for experimental animals. Thus choline was essential for weanling rats, not only for the prevention of fatty liver but also for the maintenance of tissue structure and even for their growth and survival (5,6). The absence of choline in the diet induces characteristic lesions not only in rats, but also in species as varied as mice, monkeys, ducklings, and mosquitoes (7). During the subsequent years, it became evident that choline serves as a donor of a labile methyl group in the biological system (8,9). Further biochemical studies of methyl metabolism and methyl requirements in a wide variety of biological functions have made it clear that natural sources of labile methyl are largely limited to choline, betaine, and methionine and that de novo synthesis of methyl groups is dependent upon the 280dietary provision of adequate supplies of water-soluble vitamins, especially folic acid and vitamin Β12 7,10).