Fig. 3: FAIM2 deletion exacerbates HFD-induced metabolic disorders. | Experimental & Molecular Medicine

Fig. 3: FAIM2 deletion exacerbates HFD-induced metabolic disorders.

From: Fas apoptotic inhibitor molecule 2 mitigates metabolic dysfunction-associated fatty liver disease through autophagic CRTC2 degradation

Fig. 3

a Mouse liver weight/body weight percentages of NC-fed WT mice, NC-fed KO mice, HFD-fed WT mice and HFD-fed KO mice (NC group n = 7, HFD group n = 8). b Mouse absolute serum TG, TC and LDL levels in the indicated groups (NC group n = 7, HFD group n = 8). c Images and statistics of H&E-stained (top) and Oil Red O-stained (bottom) liver sections from the indicated groups (n = 5–6). Scale bars, 50 µm. d Serum absolute ALT and AST levels in the indicated groups (NC group n = 7, HFD group n = 8). e–g Analyses of PCA (e) GSEA (f) and heatmaps (g) of livers from Faim2-KO mice fed a HFD (GSEA pathways with P < 0.05; n = 4). h Normalized mRNA levels of genes related to fatty acid metabolism in the livers of the indicated groups. Gene expression was normalized to Actb mRNA levels (n = 5). **P < 0.01; ##P < 0.01. The data are expressed as the means ± s.d. Statistical analysis was carried out via one-way ANOVA or two-tailed Student’s t-test.

Back to article page