Control of bovine hepatic fatty acid oxidation.
Fatty acid oxidation by bovine liver slices and mitochondria was examined to determine potential regulatory sites of fatty acid oxidation. Conversion of 1-[14C]palmitate to 14CO2 and total [14C]acid-soluble metabolites was used to measure fatty acid oxidation. Oxidation of palmitate (1 mM) was linear in both liver slice weight and incubation time. Carnitine stimulated palmitate oxidation; 2 mM dl-carnitine produced maximal stimulation of palmitate oxidation to both CO2 and acid-soluble metabolites. Propionate (10 mM) inhibited palmitate oxidation by bovine liver slices. Clofenapate, an inhibitor of fatty acid esterification, alone increased palmitate oxidation and was able to prevent the propionate-induced inhibition of palmitate oxidation by liver slices. Propionate (.5 to 10 mM) had no effect on palmitate oxidation by mitochondria, but malonyl Coenzyme A, the first committed intermediate of fatty acid synthesis, inhibited mitochondrial palmitate oxidation (inhibition constant = .3 microM). Liver mitochondrial carnitine palmitoyltransferase (EC 2.3.1.21) exhibited Michaelis constants for palmitoyl Coenzyme A and l-carnitine of 11.5 microM and .59 mM, respectively. Long-chain fatty acid oxidation in bovine liver is regulated by mechanisms similar to those in rats but adapted to the unique digestive physiology of the bovine.
D000818:Animals; D002417:Cattle / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism*; D066298:In Vitro Techniques; D008099:Liver / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism; D010084:Oxidation-Reduction
D005227:Fatty Acids