Studies have shown that obese mice and humans have increased serum levels of the fatty acid binding protein aP2, and that elevated aP2 levels correlate with metabolic complications. Since genetic loss of aP2 in mouse models and in humans results in lowered risk of cardiometabolic disease, the molecule offers an exciting opportunity for new intervention strategies.
Now, in a proof-of-principle study led by Broad associate member Gökhan S. Hotamisligil of the Harvard T.H. Chan School of Public Health's Sabri Ülker Center, researchers have shown that the protein may be a viable therapeutic target for type 2 diabetes. In the study, the authors identified a monoclonal antibody to aP2 that lowered fasting blood glucose, increased insulin sensitivity, and lowered both fat mass and incidence of fatty liver in obese mouse models. Their paper is published online in Science Translational Medicine.