Limitation of Long Chain Fatty Acid Oxidation in Volume Overloaded Rat Hearts
The oxidation of long chain fatty acids provides up to 70 per cent of metabolic energy to well oxygenated myocardium (CRASS et al 1969, NEELY and MORGAN 1974). This contribution to the energy production may further increase during acute exercise (CRASS et al 1969, ORAM et al 1973). However, for the rate of long chain fatty acid oxidation to be easily adjusted to the instantaneous energy requirements of the heart, the cytosolic activation and transport of activated long chain fatty acids from the cytosol to the mitochondria should not be limited. In other words, functional and unlimited carnitine acylCoA transferase and carnitine-acylcarnitine translocase (PANDE 1973, PANDE 1975, BREMER 1983) are required in order to promote the high rate of cytosolic long chain acyls translocation into the mitochondria and that of free carnitine recycling back to the cytosol (Fig.1). High myocardial content of L-carnitine is therefore necessary for the predominance of lipid metabolism in the heart to occur (NEELY and MORGAN 1974, VARY and NEELY 1982). In mechanically overloaded hearts, it has been suggested that the low tissue levels of L-carnitine, which regularly occur during the development of cardiac hypertrophy (WITTELS and SPANN 1968, REVIS and CAMERON 1979, REIBEL et al 1983, BOWE et al 1984), may impair the long chain fatty acid utilisation (BISHOP and ALTSCHULD 1971, WITTELS and SPANN 1968). This in turn could limit both the overall energy turnover and mechanical performance of chronically overloaded hearts.
KeywordsChain Fatty Acid Short Chain Fatty Acid Pressure Work 14C02 Production Free Carnitine
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