GEO series

PPARg agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein

GSE35011 Mus musculus Expression profiling by array 8 samples Submitted 2012/03/06 Platform GPL8321

Summary

Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPARγ ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPARγ ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPARγ agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes.

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Also filed as BioProject PRJNA151167. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 22405074) ↗

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