Accordingly, we demonstrated that C21-mediated improvement of insulin resistance, adipocyte differentiation, and inflammation in adipose tissue were blunted by PPARγ blockade with GW9662, supporting the idea that direct AT2 receptor stimulation by C21 ameliorated insulin resistance in T2DM model mice at least partially due to PPARγ activation. Here, PPARG is linked to type 2 diabetes mellitus.