Acetylation regulates PPARγ function

PPARγ activation by exogenous ligands, such as thiazolidinediones (TZDs), is a type 2 diabetes mellitus treatment strategy. PPARγ function can also be regulated by posttranslational modifications, such as phosphorylation, sumoylation, and ubiquitination. Jiang and colleagues report that the PPARγ is modified by acetylation, that histone deacetylase 3 (HDAC3) deacetylates PPARγ, and that HDAC3 inhibition increased expression of PPARγ target genes adiponectin and aP2, prompting adipocyte glucose uptake and insulin signalling increases. These results indicate that PPARγ acetylation is a ligand-independent mechanism of PPARγ activation, and that HDAC3 inhibition is a potential therapeutic target.

Read the full article at Jiang et al. (2014) Journal of Molecular Endocrinology 53 191–200. DOI:10.1530/JME-14-0066