As noted above, the idea that GPR119 modulation might provide the basis for an anti-obesity therapy was first suggested by the effects of its endogenous ligand, OEA, on feeding and body weight . however, reported that OEA was able to suppress food intake to a similar extent in both wild-type and GPR119-deficient mice. Nevertheless, as OEA is a relatively non-selective and low-potency GPR119 agonist, it is conceivable that its GPR119-specific effects would be masked in such a model.