American Journal of Clinical Nutrition 303 Vol. 8, May-June 1960 Mechanism of Action of Choline

I T IS obvious that an accumulation of fat such as is found in the liver of animals with cho-line deficiency may result from a change in the rate of a variety of metabolic processes. For in-stance, it may be due to an increased synthesis, a decreased oxidation in the liver, an increased mobilization from the depots to the liver or a decreased mobilization from the liver to other tissues. Accordingly, the lipotropic action of choline could be explained by a stimulation or inhibition of any one or more of such processes. During the last twenty years a number of in-vestigators have attempted to choose between these various interpretations by giving heavy water,’4 or, more recently, C’4-acetate46 to animals with or without a deficiency of choline, and then comparing the amounts and con-centrations of the newly synthesized fatty acids in the livers and depots of these two groups of animals. The results of recent experiments car-ned out in our laboratory on mice fed labeled acetate6 are essentially in agreement with those previously obtained by others. In all animals the specific activities of the fatty acids were higher in the liver than in the muscle, suggesting that the labeled fatty acids which accumulate in the liver are chiefly synthesized in this tissue rather than originating in the depots. On the other hand, no significant differences were found when the specific activities of the fatty acids in the animals receiving, or not receiving, choline were compared. This might be taken a