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Papers In Press, published online ahead of print October 24, 2000
J. Biol. Chem, 10.1074/jbc.M006246200
Submitted on July 14, 2000
Revised on October 3, 2000
Accepted on October 24, 2000
Departament Bioquímica i Biologia Molecular, University of Barcelona, Barcelona E08028
Corresponding Author: giralt{at}porthos.bio.ub.es
High expression of the peroxisome proliferator-activated receptor 
(PPAR) differentiates brown fat from white, and is related to its high capacity of lipid oxidation. We analyzed the effects of PPAR activation on expression of the brown fat-specific uncoupling protein-1 (ucp-1) gene. Activators of PPAR increased UCP-1 mRNA levels several fold both in primary brown adipocytes and in brown fat in vivo. Transient transfection assays indicated that the (-4551)UCP1-CAT construct, containing the 5' regulatory region of the rat ucp-1 gene, was activated by PPAR cotransfection in a dose-dependent manner and this activation was potentiated by Wy 14,643 and RXR. The coactivators CBP and PPAR
-coactivator-1 (PGC-1), which is highly expressed in brown fat, also enhanced the PPAR-dependent regulation of the ucp-1 gene. Deletion and point-mutation mapping analysis indicated that the PPAR-responsive element was located in the upstream enhancer region of the ucp-1 gene. This -2485/-2458 element bound PPAR and PPAR from brown fat nuclei. Moreover, this element behaved as a promiscuous responsive site to either PPAR or PPAR activation, and we propose that it mediates ucp-1 gene up-regulation associated with adipogenic differentiation (via PPAR) or in coordination with gene expression for the fatty acid oxidation machinery required for active thermogenesis (via PPAR).
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