FIGURE 7.

Model of metabolic effects of hepatic mTORC2 knock-out. Normally, mTORC2 serves to support Akt activity and thereby suppress hepatic glucose output and stimulate hepatic lipogenesis via HM phosphorylation and by facilitating PDK-mediated A-loop phosphorylation (left). When mTORC2 is lost, Akt is no longer activated, hepatic glucose output is increased, and hepatic lipogenesis is suppressed (middle). In hepatic mTORC2 knock-out mice, forced Akt activation can suppress hepatic glucose output but no longer increases lipogenesis, indicative of mTORC2 outputs that increase lipogenesis in parallel with Akt (right).