Pyruvate metabolism in the perfused rat heart

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Abstract
The metabolism of C14-labeled pyruvate in the isolated heart was studied in a closed recirculation system. Decarboxylation was the major fate of pyruvate-1-C14 and increased according to the concentration of pyruvate in the perfusion fluid. Lactate formation accounted for most of the remainder of the pyruvate-1-C14 uptake and negligible radioactivity was recovered in glycogen or tissue lipid. Comparison of the metabolism of pyruvate-1-C14 and pyruvate-2-C14 suggested that in the presence of fatty acid, oxidative decarboxylation and condensation to citric acid continued to be the principal route of entry of pyruvate into the tricarboxylic acid cycle although dilution or diversion of decarboxylated metabolites of pyruvate to nonoxidative fates was increased. Pyruvate in 5- and 10-mm concentrations reduced oxidation of palmitate-C14 and increased incorporation of palmitate into tissue lipid, specifically tissue triglyceride. The uptake and decarboxylation of pyruvate-1-C14 were less in hearts from rats fasted overnight than in hearts from rats fed ad libitum. It is proposed that oxidation of fatty acid may be the mechanism responsible for decreased utilization of pyruvate in the fasting state and other conditions in which fatty acid is the principal myocardial fuel.

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