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Am J Physiol Regul Integr Comp Physiol (February 24, 2005). doi:10.1152/ajpregu.00822.2004
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Submitted on December 3, 2004
Accepted on February 21, 2005

Hepatic {beta}-oxidation and carnitine palmitoyltransferase I in neonatal pigs following dietary treatments of clofibric acid, isoproterenol and medium chain triglycerides

Pasha Lyvers Peffer1, Xi Lin2, and Jack Odle3*

1 Animal Science, North Carolina State University, Raleigh, NC, USA; Interdepartmental Nutrition Program, North Carolina State University, Raleigh, NC, USA
2 Animal Science, North Carolina State University, Raleigh, NC, USA
3 Animal Science, North Carolina State University, Raleigh, NC, USA; Interdepartmental Nutrition Program, North Carolina State University, Raleigh, NC, USA; Functional Genomics Program, North Carolina State University, Raleigh, NC, USA

* To whom correspondence should be addressed. E-mail: jack_odle{at}ncsu.edu.

A suckling piglet model was used to study nutritional and pharmacologic means of stimulating hepatic fatty acid {beta}-oxidation. Newborn pigs were fed milk diets containing either long- or medium-chain triglycerides (MCT). The long-chain control diet was supplemented further with clofibric acid (0.5%) or isoproterenol (40 ppm), and growth was monitored for 10 to 12 d. Clofibrate increased rates of hepatic peroxisomal and mitochondrial {beta}-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 {beta}-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 {beta}-oxidation.




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