TCF7L2 and diabetes mellitus: Based on the above and our findings of decreased Tcf7l2 and increased PPARγ expression, it seems that, at least in our animal model and at the studied time point during the development of diabetes, skeletal muscles are still at least compensating partly for the developing IR, and that the compensatory pathway via Tcf7l2 may be disrupted sooner than the one via PPARγ.