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. Author manuscript; available in PMC: 2014 Dec 3.
Published in final edited form as: Cell Metab. 2013 Nov 21;18(6):10.1016/j.cmet.2013.10.011. doi: 10.1016/j.cmet.2013.10.011

Figure 6. Improvement in Insulin-induced Akt Phosphorylation and Glucose Homeostasis by CaMKII Deficiency are Abrogated by Restoring ATF4.

Figure 6

(A) HCs from Camk2gfl/fl mice were transduced with adeno-LacZ or -Cre. 24 h later, cells were incubated with tunicamycin (0.5 μg/ml) or vehicle control for 4 h. Nuclear lysates were immunoblotted for ATF4 and nucleophosmin (Np) as a loading control. (B) Nuclear ATF4 and nucleophosmin (Np) were probed in livers from DIO Camk2gfl/fl mice treated with TBG-Cre or TBG-LacZ or ob/ob mice treated with adeno-LacZ or -K43A-CaMKII. (C) HCs from Camk2gfl/fl mice were transduced with adeno-LacZ or -Cre and then 4 h later, half of the adeno-Cre transduced cells received adeno-ATF4, while the other half received adeno-LacZ control. After 24 h, the cells were incubated with palmitate and then insulin-induced p-Akt was assayed as in Figure 4. (D) As in (C), except that Trb3 mRNA was assayed by RT-qPCR (Bars with different symbols are different from each other and control, p < 0.01; mean ± S.E.M.). (E–F) Sixteen-week-old DIO mice were administered adeno-LacZ or -K43A-CaMKII, and then, two days later, half of the adeno-K43A-CaMKII mice received adeno-ATF4 while the other half received adeno-LacZ control. Livers were assayed for p-Akt, total Akt, β-actin and nuclear ATF4 and nucleophosmin (Np) by immunoblotting after insulin injection through portal vein. 5 h fasting blood glucose and plasma insulin were assayed after three weeks of treatment (Differing symbols indicate p< 0.05; mean ± S.E.M.). See also Figure S5.