A possible role for malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis.
Studied on the oxidation of oleic and octanoic acids to ketone bodies were carried out in homogenates and in mitochondrial fractions of livers taken from fed and fasted rats. Malonyl-CoA inhibited ketogenesis from the former but not from the latter substrate. The site of inhibition appeared to be the carnitine acyltransferase I reaction. The effect was specific and easily reversible. Inhibitory concentrations were in the range of values obtained in livers from fed rats by others. It is proposed that malonyl-CoA functions as both precursor for fatty acid synthesis and suppressor of fatty acid oxidation. As such, it might be an important element in the carbohydrate-induced sparing of fatty acid oxidation.
D000818:Animals; D002210:Caprylates / Q000378:metabolism; D002331:Carnitine / Q000031:analogs & derivatives / Q000378:metabolism; D003065:Coenzyme A / Q000494:pharmacology* / Q000502:physiology; D005227:Fatty Acids / Q000378:metabolism*; D007657:Ketone Bodies / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008314:Malonates; D008930:Mitochondria, Liver / Q000378:metabolism; D008954:Models, Biological; D009829:Oleic Acids / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats
D002210:Caprylates; D005227:Fatty Acids; D007657:Ketone Bodies; D008314:Malonates; D009829:Oleic Acids; D002331:Carnitine; D003065:Coenzyme A