Translational approaches: From fatty liver to non-alcoholic steatohepatitis

Figure 3 Effect of intracellular fat accumulation within the liver. Liver sensitization induces an alteration of the normal hepatic liver metabolism leading to simple steatosis with neutral triglyceride (TG) accumulation or in the more severe cases, to the production of intermediate products (DG and phospholipids) responsible for lipotoxicity. Alteration of several mediators of signaling pathways leads to the events observed during the progression from non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH) (hepatic insulin resistance, oxidative stress, inflammation, and fibrosis). IKKb: Protein Kinase-1-mediated IB Kinase; ROS: Reactive oxygen species; IL-6: Interleukin-6; TNFα: Tumor necrosis factor-α; IGF-1: Insulin-like growth factor-1; PDGF: Platelet-derivedgrowth factor; ECM: Extracellular matrix; MAPK: Mitogen-activated protein kinases; ERKs: Extracellular signal-regulated kinases; NF-κB: Nuclear factor κB.