Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction

Figure 2 Comparison of metabolic and hepatic abnormalities associated with diet-induced nonalcoholic fatty liver disease/nonalcoholic steatohepatitis in ob/ob mice. Liver weight (A), liver lipid (B), and plasma alanine aminotransferase (ALT) levels (C) of lean (C57BL6J) and ob/ob mice maintained on control low-fat diet (ob/ob LFD) or AMLN diet (ob/ob AMLN) for 12 wk; (D): Representative hematoxylin and eosin stained liver sections and quantification of percentage of liver area containing macrosteatosis; (E): Representative collagen type 1 alpha 1 stained liver sections and quantification of collagen area. Scale bar = 200 μm; (F): Representative CD68-stained liver sections and quantification of CD68-positive cells; G, H: Relative expression of genes associated with fibrosis and inflammation. ^aP ≤ 0.05, ^bP ≤ 0.01, ^cP ≤ 0.001, ^dP ≤ 0.0001 vs C57BL6J; ^eP ≤ 0.05, ^fP ≤ 0.01, ^gP ≤ 0.001, ^hP ≤ 0.0001 vs LFD. LFD: Low-fat diet.