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. Author manuscript; available in PMC: 2011 Feb 5.
Published in final edited form as: Cell. 2010 Feb 5;140(3):338. doi: 10.1016/j.cell.2010.01.001

Figure 5. Biochemical and molecular alterations in Pkr−/− tissues.

Figure 5

(A and B) Phosphorylation level of Akt on serine 473 in WAT (A) and liver (B) of Pkr+/+ and Pkr−/− mice on HFD for 20 weeks. The graphs on the right of each blot show the quantification of the results. Data are shown as the mean ± SEM. *P<0.05, **P<0.01. AU: Arbitrary unit.

(C and D) Phosphorylation level of eIF2α on serine 52 and JNK1 kinase activity, which was detected by a kinase assay using immunopurified JNK1, ATP [γ-32P] and recombinant c-Jun protein as substrate, in WAT (C) and liver (D) of Pkr+/+ and Pkr−/− mice on HFD for 20 weeks. β-Tubulin is shown as a control.

(E) Gene expression in WAT including proinflammatory cytokine levels in Pkr+/+ and Pkr−/− mice on HFD for 20 weeks.

(F and G) Haematoxylin and eosin staining of WAT (F) and liver (G) sections of Pkr+/+ and Pkr−/− mice, respectively. Scale bar, 200 μm.

(H) Triglyceride contents in liver of Pkr+/+ (n = 6) and Pkr−/− (n = 6) mice on HFD for 20 weeks.

(I) Serum alanine aminotransferase level after 6 hours daytime food withdrawal in Pkr+/+ (n = 6) and Pkr−/− (n = 6) mice on HFD for 15 weeks. Data are shown as the mean ± SEM.

See also Supplemental Figure S5.