Resolving the PPARgamma paradox

Researchers at the Dana-Farber Cancer Institute and Scripps Florida have found an alternative mechanism by which peroxisome proliferation-activated receptor-g agonists exert their antidiabetic effects.¹ By blocking phosphorylation of the protein, these compounds actually may improve insulin sensitivity independent of receptor agonism.

The findings offer a reason for drug companies to take a fresh look at antidiabetic compounds that may have been previously dismissed due to their reduced agonistic activity but now may be seen to offer therapeutic benefits with the potential for fewer side effects than marketed peroxisome proliferation-activated receptor-g (PPARG; PPARg) agonists...