Abstract

Intravenous administration of hypoglycin (L-α-amino-β-methylenecyclopropanepropionic acid) to mice resulted in hypoglycemia, which was preceded by a decrease in palmitate oxidation by myocardial homogenates from treated animals. The homogenates from treated animals carried out normal rates of glucose and hexanoate oxidation, but demonstrated depressed levels of palmityl-CoA:carnitine acyltransferase activity. The addition of carnitine to the myocardial homogenates restored both the depressed palmitate oxidation and palmityl-CoA:carnitine acyltransferase activity to normal levels. The administration of carnitine to hypoglycin-treated animals prevented the decreases in myocardial palmitate oxidation, palmityl-CoA:carnitine acyltransferase activity, and the hypoglycemia.