Steatosis as a co-factor in chronic liver diseases

Abstract

The finding of lipid accumulation in the liver, so-called hepatic steatosis or non-alcoholic fatty liver disease, is a common condition frequently found in healthy subjects. Its prevalence, in fact, has been estimated by magnetic resonance studies to be about 35% in the general population and 75% in obese persons. Nevertheless, its presence generates liver damage only in a small percentage of subjects not affected by other liver diseases. It should be defined as a "co-factor" capable of affecting severity and progression, and also therapeutic perspectives, of liver diseases to which it is associated. Herein we will evaluate the impact of hepatic steatosis and obesity on the most common liver diseases: chronic viral hepatitis C and B, and alcoholic liver disease.

Figure 1

Hypothetical physiopathological pathways leading to insulin resistance steatosis, fibrosis, hepatocellular carcinoma (HCC), apoptosis and steatosis in hepatitis C virus (HCV) infection. NS3: Non structural HCV protein 3; Core: Core HCV protein; ROS: Reactive oxygen species; TNF-α: Tumor necrosis factor α; TGF-β: Transforming growth factor β; TG: Triglycerides; LPL: Lipo-protein-lipase; SOCS3: Signaling of cytokine suppressor type 3; IRS 1-2: Insulin receptor substrate type 1 and 2.