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Originally published In Press as doi:10.1074/jbc.M107073200 on August 8, 2001

J. Biol. Chem., Vol. 276, Issue 42, 39088-39093, October 19, 2001
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Peroxisome Proliferator-activated Receptor-alpha Regulates Lipid Homeostasis, but Is Not Associated with Obesity
STUDIES WITH CONGENIC MOUSE LINES*

Taro E. AkiyamaDagger , Christopher J. NicolDagger , Catherine Fievet§, Bart Staels§, Jerrold M. Ward, Johan Auwerx||, Susanna S. T. Lee**, Frank J. GonzalezDagger , and Jeffrey M. PetersDagger Dagger Dagger §§

From the Dagger  Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, Maryland 20892, § UR545 INSERM, Département d'Athérosclérose, Institut Pasteur, 59019 Lille, France, the  Veterinary and Tumor Pathology Section, Office of Laboratory Animal Resources, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702, the || Institut de Genetique et Biologie Moleculaire et Cellulaire, CNRS, INSERM, Université Louis Pasteur, 67400 Illkirch, France, the ** Department of Biochemistry, Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, and the Dagger Dagger  Department of Veterinary Science, Center for Molecular Toxicology, Pennsylvania State University, University Park, Pennsylvania 16802-4401

Considerable controversy exists in determining the role of peroxisome proliferator-activated receptor-alpha (PPARalpha ) in obesity. Two purebred congenic strains of PPARalpha -null mice were developed to study the role of this receptor in modulating lipid transport and storage. Weight gain and average body weight in wild-type and PPARalpha -null mice on either an Sv/129 or a C57BL/6N background were not markedly different between genotypes from 3 to 9 months of age. However, gonadal adipose stores were significantly greater in both strains of male and female PPARalpha -null mice. Hepatic accumulation of lipids was greater in both strains and sexes of PPARalpha -null mice compared with wild-type controls. Administration of the peroxisome proliferator WY-14643 caused hepatomegaly, alterations in mRNAs encoding proteins that regulate lipid metabolism, and reduced serum triglycerides in a PPARalpha -dependent mechanism. Constitutive differences in serum cholesterol and triglycerides in PPARalpha -null mice were found between genetic backgrounds. Results from this work establish that PPARalpha is a critical modulator of lipid homeostasis in two congenic mouse lines. This study demonstrates that disruption of the murine gene encoding PPARalpha results in significant alterations in constitutive serum, hepatic, and adipose tissue lipid metabolism. However, an overt, obese phenotype in either of the two congenic strains was not observed. In contrast to earlier published work, this study establishes that PPARalpha is not associated with obesity in mice.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§§ To whom correspondence should be addressed: Dept. of Veterinary Science, Center for Molecular Toxicology, Pennsylvania State University, 226 Fenske Lab., University Park, PA 16802-4401. Tel.: 814-863-1387; Fax: 814-863-1696; E-mail: jmp21@psu.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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