Response of hepatic mitochondrial and peroxisomal beta-oxidation to increasing palmitate concentrations in piglets

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