Abstract

The liver component of a group of illnesses linked to metabolic dysfunction is non-alcoholic fatty liver disease (NAFLD). While fatty liver hepatitis leading to cirrhosis was identified about two decades prior, Ludwig and associates initially used the term non-alcoholic steatohepatitis (NASH) in 1980. In addition to metabolic risk factors (obesity and type 2 diabetes, in particular), excessive alcohol consumption (≥30 g/day for men and ≥20 g/day for women), and other chronic liver diseases, NAFLD is defined as the presence of steatosis in more than 5% of hepatocytes. The clinicopathological condition known as non-alcoholic fatty liver disease encompasses a broad range of liver damage, including severe fibrosis, cirrhosis, steatohepatitis, and simple steatosis. Only one stage of non-alcoholic fatty liver disease, non-alcoholic steatohepatitis is characterized pathologically by the coexistence of steatosis and necro-inflammatory activity. Steatosis is not only a possible cause of progressive liver disease on its own, but it is also a key player in the pathophysiology of several other liver illnesses. Animal models of non-alcoholic fatty liver disease (NAFLD) may be broadly classified into two groups: those resulting from genetic mutations and those exhibiting an acquired phenotype due to pharmacological or nutritional modification. In industrialized nations, NAFLD is the most frequent liver disease in children and adolescents, with a prevalence estimate of 10–40% in adults globally. Other than dietary modifications, lifestyle adjustments, and maybe bariatric surgery, there are currently no viable medical procedures that can fully cure the illness. Currently being studied are a number of tactics that aim to address pathophysiological processes such inflammation, cell damage, and the overabundance of fatty acids in the liver. Many non-invasive techniques are being researched as alternatives to or additions to biopsies, particularly in the context of follow- up monitoring.