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. 2014 Jun 2;111(24):E2482–E2491. doi: 10.1073/pnas.1323681111

Fig. 7.

Fig. 7.

Fat-specific 11β-HSD1 KO mice, and not liver-specific 11β-HSD1 KO mice, are protected from the development of CORT-induced hepatic steatosis. Frozen liver sections stained with oil red O (A) and hepatic TAG quantification (B) revealed adipose-specific 11β-HSD1 KO mice (FKO, black bars), and not liver-specific 11β-HSD1 KO mice (LKO, gray bars), were protected from CORT-induced hepatic steatosis, compared with CORT-treated WT controls (white bars). Similarly, FKO mice (and not LKO mice) were shielded from increased serum free fatty acids (C) and increased mRNA expression of key lipolytic mediators in adipose tissue (D) following CORT treatment. FKO mice were not protected from increased expression of the hepatic free fatty acid transporter CD36 induced by CORT in WT mice (E). Data were analyzed using two-way ANOVA; see Figs. S9 and S10 for the complete datasets used in the analysis (n = 6–7 in each group). *P < 0.05, ***P < 0.001 vs. WT vehicle; ∅P < 0.05, ∅∅P < 0.01 vs. WT CORT; $P < 0.05, $$P < 0.01, $$$P < 0.001 vs. LKO vehicle. C, CORT; V, vehicle.