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. Author manuscript; available in PMC: 2013 May 2.
Published in final edited form as: Cell Metab. 2012 Apr 12;15(5):739–751. doi: 10.1016/j.cmet.2012.03.002

Figure 2. CaMKII regulates glucose production and hepatic G6Pc and Pck1 expression in primary HCs.

Figure 2

(A) RNA from HCs from 3 WT and 3 Camk2g−/− mice and mouse brain from a WT mouse were probed for the indicated Camk2 isoform mRNAs by RT-PCR. (B) HCs from WT and Camk2g−/− mice were serum-depleted overnight and then incubated with forskolin (10 µm) for 14 h in serum- and glucose-free media, and then glucose in the medium was assayed (**P < 0.01 vs. WT in each group; mean ± S.E.M.). (C) HCs from WT mice were transduced with adenoviral vectors expressing LacZ, CA-CaMKII, or KD-CaMKII at an MOI of 20 and then assayed for glucose production as in (B) (*P < 0.05 and **P < 0.01 vs. LacZ in each group; mean ± S.E.M.). (D–E) HCs similar to those in (B) and (C) were serum-depleted overnight and then incubated for 5 h with 10 µM forskolin or 100 nM glucagon in serum-free media, as indicated. RNA was assayed for G6pc and Pck1 mRNA by RT-qPCR (*P < 0.05 and **P < 0.01 vs. LacZ or WT in each group; mean ± S.E.M.).