AKT1 and type 2 diabetes mellitus: In turn, these decreases in Akt activation can account for increases in hepatic gluconeogenesis in T2DM, despite the fact that there are “paradoxical” increases in hepatic lipogenic and proinflammatory pathways owing to continued or heightened activation of hepatic aPKC, and possibly other PKCs that are elevated in livers of type 2 diabetic humans.