Gut Microbiota and NAFLD

Non-alcoholic fatty liver disease (NAFLD) is characterized by an excessive intrahepatic fat accumulation, i.e., steatosis, without significant alcohol consumption. Liver steatosis is fat accumulation, in >5% of hepatocytes. NAFLD may be present in several forms ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), which is a progressive form, characterized by steatosis, hepatocytes swelling, and inflammation. Unlike simple steatosis, NASH is not reversible and can eventually progress into fibrosis, cirrhosis, or even hepatocellular carcinoma.

The first stage of alcoholic liver disease (ALD) is also characterized by hepatic steatosis. However, unlike NAFLD, the primary trigger of ALD, i.e., excessive alcohol consumption, is known and the disease is preventable. Ethanol probably does not play a prominent role in NAFLD pathogenesis but is discussed as one of the possible contributing factors. 

NAFLD is closely associated with many features of metabolic syndrome, including obesity, insulin resistance, hyperlipidemia, and hypertension, and increases the risk of cardiovascular disease and type 2 diabetes mellitus. Therefore, not surprisingly, the leading cause of death in NAFLD patients is not liver failure, but cardiovascular disease.

NAFLD is the most common chronic liver condition in the USA and Europe. Its global prevalence is rapidly increasing and is currently estimated at 24%. The highest rates are reported from the Middle East (32%) and South America (31%) and the lowest from Africa (14%). 

NAFLD pathogenesis is complex and not fully understood. The current understanding is that NAFLD is caused by a complex interplay of environmental factors mostly dietary, gut microbiota disturbances, and host factors.