Carnitine metabolism in livers and hearts of 48h-starved rats: the contribution of fat and carbohydrate to acylcarnitine formation.
The work investigated the effects of administration of 2-tetradecylglycidate (TDG), an inhibitor of mitochondrial long-chain fatty acid oxidation, alone or in combination with glucose, on concentrations of free and acylated carnitine in livers and hearts of 48 h-starved rats. The only significant effect of TDG in the heart was to decrease [short-chain acylcarnitine]. This demonstrates that in heart, fat oxidation is linked to the formation of short-chain acylcarnitine. Cardiac [short-chain acylcarnitine] was not significantly decreased by TDG if the rats were also administered glucose, suggesting that acyl CoA derived from glucose may be used for short-chain acylcarnitine formation in TDG-treated rats. TDG significantly decreased in [free carnitine]. No changes in [short-chain acylcarnitine] were observed. This indicates that formation of short-chain acylcarnitine in liver is not determined by the rates of fat oxidation. It was calculated that at least 63% of the acyl-groups esterified to carnitine were generated by intramitochondrial beta-oxidation. The effects of glucose and TDG on hepatic concentrations of free and long-chain acylcarnitine were additive, suggesting that extramitochondrial fat oxidation can contribute to acylcarnitine formation in liver.
D000818:Animals; D050260:Carbohydrate Metabolism; D002331:Carnitine / Q000031:analogs & derivatives / Q000096:biosynthesis / Q000378:metabolism*; D004852:Epoxy Compounds / Q000494:pharmacology; D005215:Fasting; D005227:Fatty Acids / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000494:pharmacology; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D004852:Epoxy Compounds; D005227:Fatty Acids; D005947:Glucose; C021756:2-tetradecylglycidic acid; D002331:Carnitine