Skip to main content
. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Pediatr Cardiol. 2011 Feb 2;32(3):323–328. doi: 10.1007/s00246-011-9889-8

Fig. 1.

Fig. 1

Both peroxisome proliferator activated receptor-alpha (PPARα) and PPAR-gamma coactivator-1alpha (PGC-1α) are activated by insulin resistance and diabetes. Forming a heterodimer with RXRα, PPARα binds to a DNA response element, namely, the nuclear receptor response element (NRRE). At binding of the NRRE within the promoter of PPAR target genes, gene transcription is activated. The transcriptional activity of PPARα is influenced by binding of endogenous ligands and by the coactivator PGC-1α. Recruiting additional coactivators with histone acetyltransferase (HAT) activity, PGC-1α interacts with other regulators such as ménage-a-trois 1 (MAT) to promote chromatin remodeling and to facilitate gene transcription