Pyruvate metabolism in the perfused rat heart

¹ Department of Medicine, Harvard Medical School, and Baker Clinic Research Laboratory, Boston, Massachusetts, and Department of Medicine, University of Toronto, Toronto, Ontario, Canada

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.

Key Words: decarboxylation • tricarboxylic acid cycle • effect of fasting on oxidation of carbohydrate substrates • effect of fatty acid on oxidation of carbohydrate substrates

Submitted on March 27, 1963

This article has been cited by other articles:

				B.-H. Park, Y. Lee, M. Walton, L. Duplomb, and R. H. Unger Demonstration of reverse fatty acid transport from rat cardiomyocytes J. Lipid Res., November 1, 2004; 45(11): 1992 - 1999. [Abstract] [Full Text] [PDF]

				R. W. Brownsey, A. N. Boone, and M. F. Allard Actions of insulin on the mammalian heart: metabolism, pathology and biochemical mechanisms Cardiovasc Res, April 1, 1997; 34(1): 3 - 24. [Full Text] [PDF]