@article{lyvers peffer_lin_jacobi_gatlin_woodworth_odle_2007, title={Ontogeny of Carnitine Palmitoyltransferase I Activity, Carnitine-Km, and mRNA Abundance in Pigs throughout Growth and Development}, volume={137}, ISSN={0022-3166 1541-6100}, url={http://dx.doi.org/10.1093/jn/137.4.898}, DOI={10.1093/jn/137.4.898}, abstractNote={Carnitine palmitoyltransferase (CPT) I catalyzes an important regulatory step in lipid metabolism; however, no studies, to our knowledge, have evaluated the molecular and kinetic [maximal velocity and Michaelis constant (K(m)) for carnitine] ontogeny of CPT I and prevailing tissue concentrations of carnitine in pigs. To this end, hepatic and skeletal muscle tissues were examined at various ages: birth; 24 h; 1, 3, 5, and 8 wk of age; and adult. Hepatic and skeletal muscle CPT I specific activities were low at birth and increased 100 and 70%, respectively, during the first week of life (P < 0.05). Skeletal muscle transcript amounts were 2.7-fold greater (P < 0.001) in 24-h-old pigs relative to newborns, whereas hepatic CPT I mRNA remained constant at each age studied. The apparent K(m) for carnitine decreased 48% (P < 0.05) during the initial 3 wk of life in liver and decreased 40% (P < 0.05) during the first week of life in skeletal muscle. Plasma and liver free carnitine concentrations increased 95 and 62%, respectively, within 24 h after birth (P < 0.05) and hepatic carnitine concentrations remained constant through 5 wk of age. Consequently, hepatic carnitine concentrations were 20-80% greater (P < 0.05) than the K(m) for carnitine during the suckling period. Skeletal muscle carnitine met or exceeded the apparent K(m) for carnitine at each stage of development. Collectively, these findings suggest that postnatal increases in CPT I activity during the suckling period are accompanied by increased tissue carnitine; however, the lack of hepatic CPT I mRNA induction and low activity reported in both tissues prior to 1 wk of age may limit postnatal lipid utilization during the piglet's transition to extra-uterine life.}, number={4}, journal={The Journal of Nutrition}, publisher={Oxford University Press (OUP)}, author={Lyvers Peffer, Pasha and Lin, Xi and Jacobi, Sheila K. and Gatlin, Lori Averette and Woodworth, Jason and Odle, Jack}, year={2007}, month={Apr}, pages={898–903} }
 @article{peffer_lin_odle_2005, title={Hepatic β-oxidation and carnitine palmitoyltransferase I in neonatal pigs after dietary treatments of clofibric acid, isoproterenol, and medium-chain triglycerides}, volume={288}, ISSN={0363-6119 1522-1490}, url={http://dx.doi.org/10.1152/ajpregu.00822.2004}, DOI={10.1152/ajpregu.00822.2004}, abstractNote={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.}, number={6}, journal={American Journal of Physiology-Regulatory, Integrative and Comparative Physiology}, publisher={American Physiological Society}, author={Peffer, Pasha Lyvers and Lin, Xi and Odle, Jack}, year={2005}, month={Jun}, pages={R1518–R1524} }