The Journal of Nutrition Vol. 127 No. 9 September 1997, pp. 1814-1821
Copyright ©1997 by the American Society for Nutritional Sciences

Rates of Mitochondrial and Peroxisomal -Oxidation of Palmitate Change during Postnatal Development and Food Deprivation in Liver, Kidney and Heart of Pigs

Xing Xian Yu^*, , James K. Drackley^{*, ,} , and Jack Odle^{*, ,}

^* Division of Nutritional Sciences and  Department of Animal Sciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801

We measured total, mitochondrial and peroxisomal capacities for -oxidation of [1-¹⁴C]palmitate in homogenates of liver, kidney and heart from pigs within 0.5 h after birth (0 h, unfed) and at 24 h (suckled or unfed), 10 d (suckled or 24-h food-deprived), 21 d (suckled or 24-h food-deprived) and 5 mo (overnight food-deprived) of age. Assays were conducted in the absence (total -oxidation) or presence (peroxisomal -oxidation) of antimycin A and rotenone. Mitochondrial -oxidation was calculated as total minus peroxisomal -oxidation. Acid-soluble products (ASP) from incubation of tissue homogenates from 24-h-old unfed pigs with [1-¹⁴C]palmitate were analyzed by radio-HPLC. Total and mitochondrial -oxidation capacities were greater (P < 0.05) at 24 h after birth in liver, and at 10 d in kidney and heart, than at 0 or 24 h. Peroxisomal -oxidation capacity was increased (P < 0.05) at 24 h after birth in liver and at 10 and 21 d in heart; in kidney, the capacity was higher during the preweaning period than in adults. Across ages, peroxisomal -oxidation capacity represented 37 to 51%, 28 to 41%, and 26 to 31% of total -oxidation capacity in liver, kidney, and heart, respectively. Food deprivation increased hepatic total -oxidation at 10 d and decreased peroxisomal -oxidation at 24 h but had no effect in kidney and heart. Regardless of the presence of respiratory inhibitors, 32%, 31 to 40%, and 45 to 50% of palmitate carboxyl carbon in acid-soluble products was accumulated in acetate in liver, kidney, and heart, respectively. We suggest that a high percentage contribution of peroxisomal -oxidation may act as a compensatory mechanism for piglets to oxidize milk fatty acids during postnatal development. Furthermore, acetogenesis may be an important fate of acetyl-CoA from -oxidation of fatty acids in various piglet tissues.

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