Fig. 7

Treatment with rmIL-22 protein inhibits gluconeogenesis in primary mouse hepatocytes via STAT3- and AMPK-dependent mechanisms. a Western blot analyses of IL-22-treated primary mouse hepatocytes. b Western blot analyses of IL-22- or insulin-treated hepatocytes. c Primary wild-type mouse hepatocytes with pre-treated PI3K or AMPK inhibitors, followed by IL-22 treatment. Primary STAT3KO mouse hepatocytes were also treated with IL-22. d The same experiments as those in panel C except all cells were pre-treated with Bt2-cAMP. In panels c and d, glucose production and gene expression were analyzed and normalized to 100 % in hepatocytes without IL-22 treatment in each group. Values represent the mean ± SEM (n = 4). *P < 0.05, **P < 0.01, and ***P < 0.001 compared with the corresponding hepatocytes without rmIL-22 treatment. ^# P < 0.05 and ^## P < 0.01 compared with the corresponding hepatocytes from vehicle + WT mice with rmIL-22 treatment