PURPOSE OF REVIEW: Non-alcoholic steatohepatitis is a liver disease characterized by steatosis and steatohepatitis in subjects whose alcohol consumption is negligible. The primary form is associated with insulin resistance whereas secondary non-alcoholic steatohepatitis occurs notably during total parenteral nutrition or in patients in the intensive care unit. This review is mainly focused on recent developments in the understanding of the pathogenesis of this disease. RECENT FINDING: Pathogenesis involves the direct role of fatty acids in liver injury, oxidative stress, cytokines, genetic susceptibility or mitochondrial dysfunction. An increased delivery of free fatty acids to the liver contributes to the first hit, originating liver steatosis. The process may undergo a second hit, characterized by inflammation and hepatocellular degeneration. Mitochondrial dysfunction plays a key role by leading to abnormal generation of reactive oxygen species, which cause lipid peroxidation. The peroxidation products and cytokines favor progression from steatohepatitis to fibrosis. Fatty liver disease may also be encountered in the intensive care unit in patients receiving parenteral nutrition. However, an adapted glucose-lipid ratio as source of non-protein calories prevents the development of fatty liver. Moreover, recent evidence suggests the importance of the type of lipid infused (structured lipid emulsion or fish oils). The acute phase response associated with severe disease can also lead to the development of fatty liver in spite of adequate nutritional support. SUMMARY: The pathogenesis of non-alcoholic steatohepatitis is multifactorial, but there is growing evidence that mitochondrial dysfunction always plays a key role. Adapted nutrition may prevent in part fatty liver in the intensive care unit.