PPARß/δ potentiates PPARγ-stimulated adipocyte differentiation KIMIHIKO MATSUSUE * , 1 , JEFFREY M. PETERS † , 1 and FRANK J. GONZALEZ * ,2 * Laboratory of Metabolism, National Cancer Institute, Bethesda, Maryland, USA; and † Department of Veterinary Science and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania, USA 2 Correspondence: Laboratory of Metabolism Building 37, Room 3106 National Cancer Institute Bethesda, MD 20892, USA. E-mail: fjgonz@helix.nih.gov <h3>SPECIFIC AIMS</h3> Based on evidence from genetic and pharmacological studies there is strong evidence that PPARγ has a central role in mediating adipocyte differentiation, yet some reports suggest that PPARß may be involved in this pathway. To specifically determine the role of PPARß in adipocyte differentiation, preadipocytes derived from wild-type and PPARß null mice were examined. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Adipocytes from wild-type mice exhibited morphology consistent with adipocyte terminal differentiation whereas adipocytes from PPARß null mice failed to differentiate after 7 days of culture in standard differentiation medium</h3> Morphological appearance of adipocytes cultured in standard differentiation medium with a PPARγ ligand showed that troglitazone significantly enhanced lipid accumulation in wild-type cells compared with cells cultured in the absence of troglitazone, and this effect was marginally
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PPARß/δ potentiates PPARγ-stimulated adipocyte differentiation
MATSUSUE, KIMIHIKO; PETERS, JEFFREY M.; GONZALEZ, FRANK J.
Follow The FASEB Journal
, Volume 18 (12): 1477
Fed of American Socs for Experimental Biology – Sep 1, 2004
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