Research Paper Volume 5, Issue 10 pp 770—781

PP2A inhibition results in hepatic insulin resistance despite Akt2 activation


Figure 2. PP2A inhibition leads to activation of insulin signaling and ensuing suppression of gluconeogenic gene transcription and gluconeo-genesis in hepatocytes. Cantharidin-treatment led to a dose-dependent increase in phosphorylation (Ser473) and activation of Akt (a). This effect was conferred onto the Akt substrate FoxO1 (Ser256), which was phosphorylated and inactivated. The inactivation of FoxO1 led to a decreased transcription of the gluconeogenic gene G6pc (c) and a reduction in the rate of gluconeogenesis (d). Fold change is relative to no treatment. Data are averages of western blot quantifications, real-time PCR results and gluconeogenesis assays ±SEM. * indicates p<0.05. Representative western blots are shown.