Fig. 4.

Switching from MCD to chow reverses steatosis but not inflammatory or fibrogenic signaling in male mice with intestinal Mttp deletion. A: Schematic diagram of experimental design. B: Biochemical quantitation of hepatic lipid content (n = 5–10/genotype). C: Representative images of Sirius red-stained liver tissue (200×) and quantitation of fibrotic area (right panel, n = 10/genotype). D: Representative images of hepatic F4/80 staining (400×) and quantitation of F4/80-stained area (right panel, n = 6/genotype). E: Relative abundance of the most abundant TG species presented as peak area ratio (n = 4/group). Right panel shows indices of lipogenesis (DNL), saturation, and elongation calculated from the relative abundance of all TG species. F: Relative abundance of hepatic ceramide (Cer) species, with total Cer peak area ratio shown on the far right. Right panel shows mRNA expression of Cer synthase isoforms in liver tissue. G: mRNA expression of genes related to fibrosis, inflammation, and lipogenesis (n = 6/genotype). H: Levels of total and phosphorylated JNK and NF-κB protein in →chow and →IKO chow liver tissue. A representative immunoblot and quantitation of relative expression are shown, with GAPDH presented as a loading control. n = 5/genotype (I) serum ALT (left) and AST levels. n = 5/genotype. J: Serum FITC-dextran FD4 levels 2 h after oral gavage. For all bar graphs, ∗P < 0.05 and ∗∗P < 0.01.