A proposed mechanism for fatty acid effects on energy metabolism of the heart.

Abstract

Abstract Long-chain acyl CoA esters can inhibit adenine nucleotide (ATP, ADP) translocation in heart mitochondria. Inhibition can be reversed by carnitine. By preventing the metabolism of long-chain fatty acids with cyanide or anerobiosis, there is an accumulation of the long-chain acyl CoA ester which in turn inhibits adenine nucleotide translocation. It is suggested that prolonged inhibition of adenine nucleotide translocation by long-chain acyl CoA esters may exert a deleterious effect on myocardial metabolism.