FIG. 13.

Serum of Nfatc2^−/− Nfatc4^−/− mice elicits increased activation in insulin signaling. HepG2 cells were challenged with serum isolated from Nfatc2^−/− Nfatc4^−/− mice (DKO) and control Nfatc2^−/+ Nfatc4^−/+ mice for the time indicated (A). Activation of Akt and S6K was determined by immunoblotting analysis using phospho-Akt (P-Akt) and phospho-S6K (P-S6K) antibodies. The extent of ERK phosphorylation was also shown. Similar amounts of Akt, S6K, ERK, and β-actin were used as controls. The effect of recombinant resistin on Akt and S6K phosphorylation (B) and AMPK activation (C) elicited by the serum of Nfatc2^−/− Nfatc4^−/− mice (DKO) and control mice was also shown.