@article{lin_shim_odle_2010, title={Carnitine palmitoyltransferase I control of acetogenesis, the major pathway of fatty acid β-oxidation in liver of neonatal swine}, volume={298}, ISSN={0363-6119 1522-1490}, url={http://dx.doi.org/10.1152/ajpregu.00634.2009}, DOI={10.1152/ajpregu.00634.2009}, abstractNote={To examine the regulation of hepatic acetogenesis in neonatal swine, carnitine palmitoyltransferase I (CPT I) activity was measured in the presence of varying palmitoyl-CoA (substrate) and malonyl-CoA (inhibitor) concentrations, and [1-14C]-palmitate oxidation was simultaneously measured. Accumulation rates of14C-labeled acetate, ketone bodies, and citric acid cycle intermediates within the acid-soluble products were determined using radio-HPLC. Measurements were conducted in mitochondria isolated from newborn, 24-h (fed or fasted), and 5-mo-old pigs. Acetate rather than ketone bodies was the predominant radiolabeled product, and its production increased twofold with increasing fatty acid oxidation during the first 24-h suckling period. The rate of acetogenesis was directly proportional to CPT I activity. The high activity of CPT I in 24-h-suckling piglets was not attributable to an increase in CPT I gene expression, but rather to a large decrease in the sensitivity of CPT I to malonyl-CoA inhibition, which offset a developmental decrease in affinity of CPT I for palmitoyl-CoA. Specifically, the IC50for malonyl-CoA inhibition and Kmvalue for palmitoyl-CoA measured in 24-h-suckling pigs were 1.8- and 2.7-fold higher than measured in newborn pigs. The addition of anaplerotic carbon from malate (10 mM) significantly reduced14C accumulation in acetate ( P < 0.003); moreover, the reduction was much greater in newborn (80%) than in 24-h-fed (72%) and 5-mo-old pigs (55%). The results demonstrate that acetate is the primary product of hepatic mitochondrial β-oxidation in Sus scrofa and that regulation during early development is mediated primarily via kinetic modulation of CPT I.}, number={5}, journal={American Journal of Physiology-Regulatory, Integrative and Comparative Physiology}, publisher={American Physiological Society}, author={Lin, Xi and Shim, Kwanseob and Odle, Jack}, year={2010}, month={May}, pages={R1435–R1443} }
 @article{xi_brown_woodworth_shim_johnson_odle_2008, title={Maternal Dietary L-Carnitine Supplementation Influences Fetal Carnitine Status and Stimulates Carnitine Palmitoyltransferase and Pyruvate Dehydrogenase Complex Activities in Swine}, volume={138}, ISSN={0022-3166 1541-6100}, url={http://dx.doi.org/10.3945/jn.108.095638}, DOI={10.3945/jn.108.095638}, abstractNote={Effects of increasing maternal L-carnitine on carnitine status and energy metabolism in the fetus were evaluated by feeding pregnant swine a corn-soybean-based diet containing either 0 or 50 mg/kg added L-carnitine (n = 10/treatment) during the first 70 d of gestation. Carnitine, carnitine palmitoyltransferase (CPT), and pyruvate dehydrogenase complex (PDHC) activities were analyzed in tissues collected from fetuses on d 55 and 70. Maternal L-carnitine supplementation increased both fetal free and long-chain carnitine concentrations by 45% in liver and free carnitine by 31% in heart tissues but did not affect kidney tissue. Elevations in free and acylcarnitines increased with gestational age from 55 to 70 d in liver but not in heart and kidney. The increased carnitine concentrations resulted in a 45% increase in PDHC activity in heart and liver on d 70 of gestation but did not affect kidney and liver on d 55 of gestation. The increases in carnitine concentrations were accompanied by a 70% increase in hepatic CPT activity in 70-d-old fetuses, but activities in heart and kidney were unaffected. The Michaelis constant (K(m)) of CPT for carnitine in fetal tissues was not influenced by carnitine supplementation (P > 0.1). Notably, the concentrations of carnitine measured on d 70 were only 25-40% of the K(m) values in liver, 60-70% in heart, and 30-40% in kidney (P < 0.001). We conclude that carnitine ingestion during pregnancy increases fetal carnitine concentrations and stimulates heart PDHC and liver CPT activity without altering carnitine K(m).}, number={12}, journal={The Journal of Nutrition}, publisher={Oxford University Press (OUP)}, author={Xi, Lin and Brown, Kelly and Woodworth, Jason and Shim, Kwanseob and Johnson, Bradley and Odle, Jack}, year={2008}, month={Dec}, pages={2356–2362} }