The Effect of Insulin and Deprivation of Food on Metabolism of Acetoacetic Acid by Muscle.

Previously our laboratory demonstrated that voluntary muscle fiber groups and diaphragms from depanereatized and alloxan-diabetic rats take up leas acetoacetic acid than fiber groups and diaphragms from control animals (1, 2). The addition of glucose and insulin causes an increase in acetoacetic acid uptake by muscle fiber groups from both control and depancreatized rats. These experiments were performed on muscle from both fed rats and rats that had been deprived of food for 24 hours. It was concluded that the decrease in ketone body utilization by muscle from insulin-deficient animals is a contributing factor in diabetic ketosis. These conclusions have been further substantiated by Scow and Chernick (3), who reported that the utilization of both acetoacetic and /3-hydroxybutyric acid is reduced in insulin-deficient rats. &reeve (4) followed the conversion of acetate-l-% to ketone bodies in diabetic patients and also presented evidence in support of impaired utilization of P-hydroxybutyric acid. It has been demonstrated, by measuring patterns of enzyme activity, that the pathways by which the major portion of the ketone bodies are produced in liver differ in the ketosis associated with deprivation of food and that found in diabetic rats (5). The present paper reports an investigation of the effect of prolonged deprivation of food on the uptake of acetoacetic acid by diaphragms and skeletal muscle fiber groups of rats and the effect of insulin’ on the uptake of acetoacetate-3-14C2 and its conversion to l-4C02 by these muscles.