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Brown Remodeling of While Adipose Tissue by
SirT1-dependent Deacetylation of PPARγ
Qiang et al
A novel mechanism has been defined for controlling peroxisome proliferator-activated receptors γ(PPARγ) activity in response to thiazolidinedione (TZD) ligands, in which deacetylation of PPARγ by SirT1 remodels the transcriptional complex. This change favors expression of genes associated with increased energy use and insulin sensitization in white adipose tissue (WAT), and is required for a portion of the beneficial effects of TZDs. More broadly, PPARγ acetylation and other recently identified regulatory modifications are clarifying the mechanisms by which TZDs exert their antidiabetic effects in fat cells and other tissues.
PPARγ is a ligand-activated transcription factor first studied for its importance in adipogenesis. From then, it has become recognized that PPARγ also mediates diverse effects in nonadipose tissues including liver, skeletal muscle, brain, bone, and blood vessels. PPARγ is thought to be a fatty acid and lipid sensor, which when activated can stimulate expression of genes that promote insulin action, fatty acid …