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Control of Bovine Hepatic Fatty Acid Oxidation¹

Department of Animal Science, Michigan State University, East Lansing 48824

ABSTRACT

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 µM). Liver mitochondrial carnitine palmitoyltransferase (EC 2.3.1.21) exhibited Michaelis constants for palmitoyl Coenzyme A and 1-carnitine of 11.5 µM 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.

¹ Published with approval of the Director of the Agricultural Experiment Station as Journal Article Number 11783.

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