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

Figure 5 Mitochondria from ob/ob AMLN livers display reduced respiratory capacity and increased proton leak. (A): Oxygen consumption of primary hepatocytes isolated from C57BL6J, ob/ob LFD and ob/ob AMLN livers normalized to mitochondrial content (citrate synthase activity, CSA). Changes in mitochondrial respiration in response to oligomycin, FCCP and antimycin A are shown. Light grey box = basal respiration, dark grey box = maximal uncoupled respiration; (B): Quantification of baseline oxygen consumption (basal respiration) and FCCP-stimulated oxygen consumption (maximal respiration) normalized to CSA; (C): Mitochondrial respiratory control ratio, a measure of mitochondrial coupling, defined as state 3/ state o respiration of mitochondria isolated from the livers of C57BL6J, ob/ob LFD and ob/ob AMLN mice; (D): Mitochondrial leaking control ratio, a measure of proton leak, defined as state o/ state 3_U respiration. ^aP ≤ 0.05, ^bP ≤ 0.01, vs C57BL6J; ^fP ≤ 0.01, ^gP ≤ 0.001, vs LFD. LFD: Low-fat diet.