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The nuclear receptor, NR1C2 or peroxisome proliferator-activated receptor (PPAR)-  δ  , is ubiquitously expressed and important for placental development, fatty acid metabolism, wound healing, inflammation, and tumour development. PPAR  δ   has been hypothesized to function as both a ligand activated transcription factor and a repressor of transcription in the absence of agonist. In this paper, treatment of mice conditionally expressing human PPAR  δ   with GW501516 resulted in a marked loss in body weight that was not evident in nontransgenic animals or animals expressing a dominant negative derivative of PPAR  δ  . Expression of either functional or dominant negative hPPAR  δ   blocked bezafibrate-induced PPAR  α  -dependent hepatomegaly and blocked the effect of bezafibrate on the transcription of PPAR  α   target genes. These data demonstrate, for the first time, that PPAR  δ   could inhibit the activation of PPAR  α  in vivo  and provide novel models for the investigation of the role of PPAR  δ   in pathophysiology.

Conditional Expression of Human PPARδand a Dominant Negative Variant of hPPARδ In Vivo