Lipid metabolism in the newborn heart.

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Abstract
In recent years, long chain fatty acids (LCFA) have been shown to the major metabolic fuel of the adult heart. In the developing mammalian heart, however, evidence has been obtained that carbohydrates are the primary source of energy. A study was undertaken to elucidate the biochemical basis of this age dependent difference in cardiac metabolism. Cardiac homogenates from newborn rats (< 1 day old) oxidized glucose-U-C14 at a rate 10-fold greater than those of adults (N=1.65; A=0.17 [mu]moles/g protein/30 min.). The ability of the newborn heart to oxidize palmitate-1-C14, however, was only 15% of the adult (N=0.94; A=6.12). The limited capacity of LCFA oxidation by newborn heart was correlated with: decreased LCFA activation (LCF acyl thickinase activity), decreased LCF acyl CoA-carnitine transferase activity, and decreased concentration of carnitine. LCF acyl CoA-carnitine transferase and carnitine serve to effect a translocation of activated LCF acyl groups into mitochondria where the FA undergoes oxidation. Whereas LCFA oxidation was decreased in the newborn, incorporation of palmitate-1-C14 into glycerides and phospholipids greatly exceeded that in the adult. This indicated that LCFA activation was probably not rate limiting in palmitate oxidation. Correction of the carnitine lack in vitro tripled the palmitate rate of oxidation, but failure to attain the adult level of oxidation indicated that the transferase activity was probably the rate controlling step in LCFA oxidation by the newborn heart. Non-depressed rates of hexamoate-1-C14 and of succinate-2,3-C14 oxidation indicated no impairment in activity of [beta] -oxidation or in the activity of the Krebs cycle or the electron transport chain in the newborn heart. The observations imply an age dependent evolution of substrate choice by the heart which is under enzymatic control.