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Am J Physiol Endocrinol Metab 284: E351-E356, 2003. First published October 8, 2002; doi:10.1152/ajpendo.00354.2002
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Vol. 284, Issue 2, E351-E356, February 2003

Quantitative assessment of anaplerosis from propionate in pig heart in vivo

Wenjun Z. Martini1,2, William C. Stanley1,2, Hazel Huang1, Christine Des Rosiers3, Charles L. Hoppel4, and Henri Brunengraber2

Departments of 1 Physiology and Biophysics, 2 Nutrition, and 4 Pharmacology and Medicine, Case Western Reserve University, Cleveland, Ohio 44106-7139; and 3 Department of Nutrition, University of Montreal, Montreal, Quebec, Canada H3C 3J7

Normal cardiac metabolism requires continuous replenishment (anaplerosis) of catalytic intermediates of the citric acid cycle. Little is known about the quantitative aspects of propionate as a substrate of in vivo anaplerosis; therefore, we measured the rate of propionate entry into the citric acid cycle in hearts of anesthetized pigs. [U-13C3]propionate (0.25 mM) was infused in a coronary artery branch for 1 h via an extracorporeal perfusion circuit, and cardiac biopsies were analyzed for the mass isotopomer distribution of citric acid cycle intermediates. Infusion of propionate did not affect myocardial oxygen consumption, heart rate, or contractile function. In the infused territory, propionate infusion did not affect uptake of glucose and lactate but decreased free fatty acid uptake by one-half (P < 0.05). Propionate extraction and uptake were 57.4 ± 3.3% and 0.078 ± 0.009 µmol · min-1 · g-1. Anaplerosis from propionate, calculated from the mass isotopomer distribution of succinate, accounted for 8.9 ± 1.3% of the citric acid cycle flux. Propioylcarnitine release accounted for only 0.033 ± 0.002% of propionate uptake. Methylcitrate did not accumulate. Thus administration of a low concentration of propionate appears to be a convenient and safe way to boost anaplerosis in the heart.

tricarboxylic acid cycle; cataplerosis; mass isotopomer analysis; mass spectrometry


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