Hepatic β-oxidation and carnitine palmitoyltransferase I in neonatal pigs after dietary treatments of clofibric acid, isoproterenol, and medium-chain triglycerides

Abstract

A suckling piglet model was used to study nutritional and pharmacologic means of stimulating hepatic fatty acid β-oxidation. Newborn pigs were fed milk diets containing either long- or 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 β-oxidation of [1-14C]-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 β-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 β-oxidation.