Figure 4. Loss of Slc39a5 improves liver function and steatosis in leptin-receptor deficient female mice and in female mice challenged with high-fat high fructose diet (HFFD).
Slc39a5-/-;Lepr-/- and corresponding control mice (A–F) were sacrificed after 16 hr fasting at 34 wk of age. (G–L) Slc39a5-/- and Slc39a5+/+ mice were fed HFFD or NC for 30 wk and sacrificed after 16 hr of fasting. (A, G) Representative images of livers stained with H&E. Scale bar, 200 µm. (B, H) Hepatic triglyceride (TG) content in explanted liver samples at an endpoint. (C, I) Serum ALT. (D, J) Serum AST. (E, K) Non-alcoholic fatty liver disease (NAFLD) activity score, (F, L) Hepatic beta-hydroxybutyrate (BHOB). *p<0.05, **p<0.01, ***p<0.001, Slc39a5-/-;Lepr-/- and corresponding control mice: one-way ANOVA with post hoc Tukey’s test, HFFD or NC: two-way ANOVA with post hoc Tukey’s test. Numeric data is summarized in Supplementary file 4 and Supplementary file 5.
Figure 4—figure supplement 1. Loss of Slc39a5 improves liver function and steatosis in Lepr-/- male mice and reduces hepatic triglyceride in male mice challenged with high-fat high fructose diet (HFFD).
