ABSTRACT
The liver is the major gland in the body involved in the intermediate metabolism of nutrients absorbed from the intestine. For this reason, it is intuitive to think that this organ could be vulnerable to metabolic stress. However, the definition, the pathogenesis, the natural history, and the clinical features of metabolic-induced liver damage have been identified only in the past 10 years. For example, liver steatosis or fatty liver (FL), an infiltration of fat inside the hepatocyte, has been traditionally considered a benign and reversible condition, usually the expression of a nonspecific response of the liver to metabolic stress of different origin. In the light of new knowledge, steatosis, especially macrosteatosis, is increasingly recognized as a condition that could evolve to cirrhosis and HCC, and its etiology is correlated not just to alcohol abuse. As shown in Figure 5.1, FL may progress to fibrosis and cirrhosis both in alcoholic liver disease (left panel) and in nonalcoholic liver disease (right panel), with possible shunting that could rapidly worsen the disease when acute hepatitis occurs.
