Fig. 7

Higher Menin expression activates the insulin pathway and AMPK signaling pathway but inhibits the activity of Akt and PPARγ, facilitating glucose uptake and gluconeogenesis while suppressing fatty acid uptake and adipogenesis. A. Representative Western blot results of key mediator factors involved in the insulin receptor (activated IRS1 being phosphorylated at S307, and its total protein), Akt (activated Akt being phosphorylated at S437, and its total protein), AMPK (activated AMPK being phosphorylated at T172, and its total protein), PPARγ (activated PPARγ being phosphorylated at S273, and its total protein), and GSK3β (activated GSK3β being phosphorylated at T216, and its total protein) upon Menin overexpression in hepatocytes. B. Quantitative results of Western blot results obtained from three independent experiments, indicating enhanced activity of IRS1, AMPK, and/or GSK3β, but inhibited activity of Akt and/or PPARγ. C. Representative Western blot results of downstream factors involved in the PPAR signaling pathway upon Menin overexpression in hepatocytes, showing significantly inhibited fatty acid transporter CD36 but significantly elevated rate-limiting enzyme of glucose uptake GK and gluconeogenesis PCK. D. Quantitative results of Western blot results from three independent experiments, indicating that higher Menin expression suppresses fatty acid uptake (CD36) while facilitating glucose uptake (GK) and gluconeogenesis (PCK)