Rates of mitochondrial and peroxisomal β-oxidation of palmitate change during postnatal development and food deprivation in liver, kidney and heart of pigs

We measured total, mitochondrial and peroxisomal capacities for β- 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 β-oxidation) or presence (peroxisomal β-oxidation) of anti-mycin A and rotenone. Mitochondrial β-oxidation was calculated as total minus peroxisomal β-oxidation. Acid-soluble products (ASP) from incubation of tissue homogenates from 24-hold unfed pigs with [1-¹⁴C]palmitate were analyzed by radio-HPLC. Total and mitochonddal β-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 β-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 β-oxidation capacity represented 37 to 51%, 28 to 41%, and 26 to 31% of total β-oxidation capacity in liver, kidney, and heart, respectively. Food deprivation increased hepatic total β-oxidation at 10 d and decreased peroxisomal β-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 palmirate 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 β-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 β-oxidation of fatty acids in various piglet tissues.