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Am J Physiol Regul Integr Comp Physiol (January 13, 2005). doi:10.1152/ajpregu.00751.2004
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Submitted on November 4, 2004
Accepted on January 10, 2005

Induction of overlapping genes by fasting and a peroxisome proliferator in pigs: Evidence of functional PPAR {alpha} in non-proliferating species

Yewon Cheon1, Takayuki Y Nara2, Mark R Band3, Jonathan E Beever4, Matthew A Wallig5, and Manabu T Nakamura6*

1 Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
2 Department of Food Science & Human Nutrition, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
3 Biotechnology Center, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
4 Department of Animal Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
5 Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Department of Veterinary Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
6 Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Department of Food Science & Human Nutrition, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA

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

Peroxisome proliferators activated receptor {alpha} (PPAR{alpha} ), a key regulator of fatty acid oxidation, is essential for adaptation to fasting in rats and mice. However, physiological functions of PPAR{alpha} in other species, including humans, are controversial. A group of PPAR{alpha} ligands called peroxisome proliferators (PPs) causes peroxisome proliferation and hepatocarcinogenesis only in rats and mice. To elucidate the role of PPAR{alpha} in adaptation to fasting in non-proliferating species, we compared gene expressions in pig liver from fasted and clofibric acid (a PP)-fed groups against a control diet-fed group. As in rats and mice, fasting induced genes involved with mitochondrial fatty acid oxidation and ketogenesis in pigs. Those genes were also induced by clofibric acid feeding, indicating that PPAR{alpha} mediates the induction. In contrast to rats and mice, little or no induction of genes for peroxisomal or microsomal fatty acid oxidation was observed in clofibric acid-fed pigs. Histology showed no significant hyperplasia or hepatomegaly in the clofibric acid-fed pigs, whereas it showed a reduction of glycogen by clofibric acid, an effect of PPs also observed in rats. Copy number of PPAR{alpha} mRNA was higher in pigs than in mice and rats, suggesting that peroxisomal proliferation and hyper-response of several genes to PPs seen only in rats and mice are unrelated to the abundance of PPAR{alpha}. In conclusion, PPAR{alpha} is likely to play a central role in adaptation to fasting in pig liver as in rats and mice.




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