PPARγ: no SirT, no service.

A novel mechanism has been defined for controlling PPARγn activity in response to thiazolidinedione ligands, in which deacetylation of PPARγ by SirT1 remodels the transcriptional complex. This change favors expression of genes associated with increased energy utilization and insulin sensitization in white adipose tissue, and is required for a portion of the beneficial effects of thiazolidinediones. More broadly, PPARγ acetylation and other recently identified regulatory modifications are clarifying the mechanisms by which thiazolidinediones exert their antidiabetic effects in fat cells and other tissues.