Together these results suggest that, consistent with the results from the STZ-induced T1DM mice, in vivo inhibition of AR in T2DM db/db mice also lead to dephosphorylation of both ERK1/2 and PPARα, which might eventually lead to the activation of hepatic PPARα to significantly affect hepatic lipid metabolism. The gene discussed is PPARA; the disease is type 1 diabetes mellitus.