The liver is the key organ for lipid metabolism, as lipids may accumulate primarily in hepatocytes, if there is an imbalance between the delivery of fat to the liver from adipose tissue stores and the export of fat as a component of very-low-density lipoproteins.

Physiologically, when examined by electron microscopy or fat stains, small lipid droplets can be seen in the cytoplasm of hepatocytes. However, in pathological conditions of metabolic imbalance, stress, or cellular injury, lipid droplets become magnified and can be visualized by light microscopy as clear vacuoles in hepatocytes cytoplasm.

Therefore, it is evident that obesity and metabolic syndrome cause alteration in the liver and its role in lipid and energy metabolism which in turn leads to series of histopathologic changes. Histologically, the fatty liver or steatosis is caused by a rise in hepatocellular fat vacuoles triggered by increased body mass index. Moreover, small number of steatotic hepatocytes, disintegrate and release liver enzyme which further leads to focal nonspecific inflammation.

Steatohepatitis is the stage with cytoskeletal damage in genetically susceptible individuals causing loss of normal keratin filaments, ballooning degeneration of affected liver cells, and formation of Mallory-Denk bodies. Additionally, hepatic stellate cells get triggered and produces intralobular fibrosis in the perisinusoidal spaces, whereas periportal ductular reaction stimulates portal myofibroblasts and periportal fibrosis in patients with steatohepatitis. This process of continuous fibrogenesis, causes progression of fibrosis to cirrhosis. Furthermore, cirrhotic liver may cause development of hepatocellular carcinoma. However, both hepatocellular adenoma and hepatocellular carcinoma can even occur in fatty liver disease before its progression to cirrhosis.

Source: Goodman ZD. The Impact of Obesity on Liver Histology. Clin Liver Dis . 2014 Feb;18(1):33-40.