Dietary Lipid and Postnatal Development. II. Palmityl Coenzyme A Oxidation in Heart and Liver

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Abstract
Extract: There is only indirect evidence to suggest that the sudden postpartum appearance of dietary lipid regulates the perinatal development of the enzyme pathways required for fatty acid oxidation. To test this idea directly, rabbit pups were maintained on diets containing lipid to equal either 14.2% (LF) or 77.6% (HF) of the total caloric intake. Palmityl coenzyme A oxidation rates in the presence of excess ADP and carnitine were measured polarographically in heart and liver homogenates. No significant difference in oxidation rates between HF and LF groups was observed even at 10 days of age. Palmityl coenzyme A oxidation in both groups was carnitine dependent and was in general the same as that of mother-fed animals. Similarly, an evaluation of cytochrome oxidase activity and glutamate + malate-supported respiration in heart and liver homogenates revealed no difference attributable to diet. To consider the possibility that fatty acid oxidation might be specifically increased or decreased over other mitochondrial respiratory activity as a function of diet, palmityl coenzyme A oxidation rates were normalized with respect to glutamate + malate oxidation rates. A similar comparison was made relative to cytochrome oxidase activity. Still no differences were observed between HF and LF groups. By studying the maximum rate of oxygen utilization in the presence of excess carnitine and palmityl-coenzyme A we would have detected any change in a rate-limiting step for fatty acid oxidation beyond acyl activation. We must conclude, therefore, that large differences in the proportion of postnatal dietary lipid do not influence the cellular capacity to oxidize palmityl coenzyme A. Speculation: We found no evidence to support the suggestion that the ability to oxidize long chain fatty acids is influenced by the amount of lipid in the postnatal diet. It seems likely that factors other than dietary lipid may be more important in regulating perinatal oxidative energy metabolism.