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J R Aprille

Publications and source records attributed to J R Aprille.

62 records · Page 4Linked to original sources
PubMed1977

Liver and skeletal muscle mitochondrial function following burn injury.

The possibility of altered mitochondrial function consequent to burn injury was investigated. Mitochondria isolated from liver or skeletal muscle of burn-injured rats (20% tbs) were compared at 3 days postburn to shams and normal controls. Mitochondrial yields were the same for all groups. ADP;O ratios were in the theoretical ranges expected and did not differ among burn, sham, and normal animals. Respiratory control ratios (RCR's) were decreased in liver mitochondria, averaging 71.7% of normal for burned animals compared to 95.8% for the sham group. The loss of respiratory control in liver mitochondria implies inefficient use of substrate chemical energy and could contribute to postburn hypermetabolism. The different response of muscle mitochondria as compared to liver suggests that alterations may be organ specific.

Adenosine Diphosphate↗
PubMed1976

Dietary lipid and postnatal development. I. A model for neonatal studies requiring high and low fat diets from birth.

As a prerequisite to a biochemical investigation into the role of dietary lipids in regulating perinatal fatty acid metabolism, we developed and evaluated a model in which the amount of lipid in the diet can be easily controlled from birth to at least 10 days of age. Neonatal rabbits were fed purified equicaloric diets in which lipid supplied either 14.2% or 77.6% of the total calories. Mortality due to all causes was about 40% in both groups. Some differences in physical development between the two groups were noted. Animals receiving the smaller amount of lipid (LF group) gained weight to 150% birth weight day 10, whereas the group receiving the larger amoung of lipid (HF group) did not gain. In addition, the HF group had lower body temperatures, smaller liver and kidney weights, and greater brain weights relative to body weight. These differences are discussed in relation to the composition of the HF and LF diets. The model promises to provide a direct approach to a more precise evaluation of varied dietary regimens in the neonatal period. In particular, the model lends itself to studies relating diet to developing biochemical functions. In an accompanying paper, we report the results of an investigation comparing fatty acid oxidation in heart and liver of neonates fed the HF and LF diets described here.

Animals↗
PubMed1976

Dietary lipid and postnatal development. II. Palmityl coenzyme A oxidation in heart and liver.

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 no influence the cellular capacity to oxidize palmityl coenzyme A.

Adenosine Diphosphate↗