Effect of palmitoyl-CoA and β-oxidation of fatty acids on the kinetics of mitochondrial citrate transporter

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Abstract
The kinetics of rat hepatic mitochondrial citrate transporter were studied using 1,2,3-benzene tricarboxylate and the inhibitor-stop technique at 8.degree. C. The apparent Km for this transporter was 250 .mu.M and the maximum velocity was 2 nmol of citrate transported/min per mg of mitochondrial protein. This apparent Km was increased when hepatic mitochondria were preincubated with both L-palmitoylcarnitine and CoA-SH but not with either alone. This rise in apparent Km was accompanied by a rise in the acid insoluble CoA-SH content. Removal of mitochondrial and insoluble CoA by defatted albumin resulted in a parallel decrease in the apparent Km. The apparent Km for the citrate transporter was increased after coupled .beta.-oxidation of L-palmitoylcarnitine or octanoate without a detectable increase in acid insoluble CoA. Inhibition of .beta.-oxidation of L-palmitoylcarnitine by the D-derivative prevented the rise in the apparent Km. Preincubation with ATP resulted in an increase in this apparent Km. When L-palmitoylcarnitine oxidation occurred without ATP accumulation (hexokinase, glucose, ADP and inorganic phosphate) the apparent Km for the citrate transporter increased 2-3 fold. The apparent Km for the citrate transporter varied directly with the acid insoluble CoA content. This Km was increased as a result of .beta.-oxidation of fatty acids but the mechanism was not solely attributable to a rise in acid insoluble CoA or ATP. The physiological implications of these findings are discussed.

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