CALL FOR PAPERS Regulation of Lipid Metabolism and of Insulin Sensitivity by PPARs Hepatic -oxidation and carnitine palmitoyltransferase I in neonatal pigs after dietary treatments of clofibric acid, isoproterenol, and medium-chain triglycerides

Peffer, Pasha Lyvers, Xi Lin, and Jack Odle. Hepatic -oxidation and carnitine palmitoyltransferase I in neonatal pigs after dietary treatments of clofibric acid, isoproterenol, and medium-chain triglycerides. Am J Physiol Regul Integr Comp Physiol 288: R1518–R1524, 2005. First published February 24, 2005; doi:10.1152/ajpregu.00822.2004.—A suckling piglet model was used to study nutritional and pharmacologic means of stimulating hepatic fatty acid -oxidation. Newborn pigs were fed milk diets containing either longor medium-chain triglycerides (LCT or MCT). The long-chain control diet was supplemented further with clofibric acid (0.5%) or isoproterenol (40 ppm), and growth was monitored for 10–12 days. Clofibrate increased rates of hepatic peroxisomal and mitochondrial -oxidation of [1-C]palmitate by 60 and 186%, respectively. Furthermore, malonyl-CoA sensitive carnitine palmitoyltransferase (CPT I) activity increased 64% (P 0.05) in pigs receiving clofibrate. Increased CPT I activity was not congruent with changes in message, as elevated abundance of CPT I mRNA was not detected (P 0.16) when assessed by qRT-PCR. Neither rates of -oxidation nor CPT activities were affected by dietary MCT or by isoproterenol treatment (P 0.1). Collectively, these findings indicate that clofibrate effectively induced hepatic CPT activity concomitant with increased fatty acid -oxidation.