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. Author manuscript; available in PMC: 2017 May 1.
Published in final edited form as: Clin Liver Dis. 2016 Feb 18;20(2):245–262. doi: 10.1016/j.cld.2015.10.007

Figure 7. Consequences of increased hepatocellular uptake and oxidation of LCFA in obesity.

Figure 7

Many of the features of NASH follow logically from the increase in hepatocellular LCFA uptake and subsequent increase in the generation of reactive oxygen species (ROS) by mitochondrial and extra-mitochondrial LCFA oxidation. These, in turn, lead to generation of intracellular mediators such as MDA, HNE, TNFα, TGFβ, leptin, and IL8, which – in turn – cause several of the characteristic histologic features of NASH. ROS resulting from EtOH oxidation lead to generation of some of the same mediators, potentially explaining the histologic similarity between NASH and alcoholic hepatitis. Adapted from Bradbury MW, Berk PD. Lipid metabolism in hepatic steatosis. Clin Liver Dis 2004; 8:639-671, with permission.