Propionyl L-carnitine improvement of hypertrophied heart function is accompanied by an increase in carbohydrate oxidation.

Abstract

Propionyl L-carnitine (PLC) is a naturally occurring derivative of L-carnitine that can improve hemodynamic function of hypertrophied rat hearts. The mechanism(s) responsible for the beneficial effects of PLC is not known, although improvement of myocardial energy metabolism has been suggested. In this study, we determined the effect of PLC on carbohydrate and fatty acid metabolism in hypertrophied rat hearts. Myocardial hypertrophy was produced by partial occlusion of the suprarenal aorta of juvenile rats. Over a subsequent 8-week period, a mild hypertrophy developed, resulting in a 17% increase in heart weight in these animals compared with the sham-operated control animals. Myocardial carnitine was decreased in hypertrophied hearts compared with hearts from sham-operated animals (4155 +/- 383 versus 5924 +/- 570 nmol.g dry wt-1, respectively; P < or = .05). Perfusion of isolated working hearts for 60 minutes with buffer containing 1 mmol/L PLC increased carnitine content in hypertrophied hearts from 4155 +/- 383 to 7081 +/- 729 nmol.g dry wt-1 (P < or = .05). In the presence of 1.2 mmol/L palmitate, fatty acid oxidation rates were not decreased in the hypertrophied hearts compared with control hearts. PLC treatment did not alter rates of fatty acid oxidation in control hearts but did result in a small increase in rates in the hypertrophied hearts.(ABSTRACT TRUNCATED AT 250 WORDS)