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. 2016 Dec 19;6(2):206–218. doi: 10.1016/j.molmet.2016.12.005

Figure 6.

Figure 6

Evaluation of insulin signaling and mediators of the inflammatory and unfolded protein response (UPR) pathways in iNOS KO mice treated with PBA. (A) Insulin-induced Protein kinase B (Akt) phosphorylation in liver and epididymal adipose tissue. (B and C) Akt phosphorylation densitometry in (B) liver and (C) adipose tissue. (D) c-JunN-terminal kinase (JNK) phosphorylation in liver and epididymal adipose tissue. (E and F) JNK phosphorylation densitometry in (E) liver and (F) adipose tissue. (G and H) IRE-1α mRNA expression in (G) liver and (H) adipose tissue. (I and J) PERK mRNA expression in (I) liver and (J) adipose tissue. ˆp < 0.05 vs. iNOS KO HFD, #p < 0.05 vs. iNOS KO PBA HFD. Bars represent mean ± SEM from 4 to 8 mice. Similar results were observed when using delta percentage of baseline.