| [ Summary ] |
Non‒alcoholic fatty liver disease (NAFLD) including non‒alcoholic steatohepatitis (NASH), which is recognized as an aggressive form of NAFLD, is considered a hepatic manifestation of metabolic syndrome. NAFLD is now recognized as a leading cause of global morbidity and mortality in chronic liver disease in relation to the "obesity pandemic". NAFLD can progress to cirrhosis, hepatic failure, and hepatocellular carcinoma. Patients presenting with NAFLD show quantitative and qualitative changes in the composition of their intestinal microbiome. Furthermore, patients presenting with NAFLD show increased intestinal permeability and elevated systemic levels of gut‒derived microbial products. Maintaining eubiosis, stabilizing the gut mucosal barrier, and/or preventing cellular responses to microbial products protect from experimental animal models with NAFLD. Therefore, intestinal dysbiosis and pathological bacterial translocation appear to be the primary mechanisms related to the pathogenesis of NAFLD, similar to the situation observed in patients presenting with alcoholic liver disease. Regarding the mechanisms causing intestinal dysbiosis, bacterial translocation, and their interactions are being gradually understood. Moreover, effective management of intestinal microbiota is now anticipated to be one of the most useful therapeutic options to treat NAFLD. |