Response of Hepatic Mitochondrial and Peroxisomal β-Oxidation to Increasing Palmitate Concentrations in Piglets

Responses of total, mitochondrial, and peroxisomal μ-oxidation to increasing [1-¹⁴C]-palmitate concentrations (0.02–1.0 m>M) were measured in liver homogenates from neonatal pigs. Incubations were conducted in the absence (total μ-oxidation) or presence (peroxisomal μ-oxidation) of antimycin A and rotenone; mitochondrial μ-oxidation was calculated as total minus peroxisomal oxidation. Total and mitochondrial μ-oxidations were maximized at a palmitate concentration of 0.05 mM, whereas peroxisomal μ-oxidation was maximized at 0.50 mM palmitate. Across concentrations, peroxisomal μ-oxidation contributed 40–47% of total μ-oxidation. An increased rate of CO₂ production and a greater ratio of CO₂ production to total mitochondrial μ-oxidation as palmitate concentration increased suggested that the limited capacity for mitochondrial μ-oxidation was attributable primarily to limited ketogenic capacity. Comparative observations in liver from adult rats showed that peroxisomal μ-oxidation was maximized at 0.1 mM palmitate, but total and mitochondrial μ-oxidation rates were not maximized even at 1 mM palmitate. At 1 mM palmitate, peroxisomal μ-oxidation was 20% of total μ-oxidation in adult rats and 37% in adult pigs. Therefore, the contribution of peroxisomal μ-oxidation to total μ-oxidation is highly dependent on substrate concentration and appears to be greater in adult pigs than in adult rats. The greater proportional contribution of peroxisomal μ-oxidation in piglet liver might act as a compensatory mechanism for piglets to oxidize milk fatty acids.