The prevalence of non-alcoholic fatty liver disease (NAFLD) in different countries ranges from 10–24% in the general population and reaches 55–74% among individuals with excess body weight. Numerous studies have demonstrated that NAFLD, including non-alcoholic steatohepatitis (NASH), is closely associated with components of metabolic syndrome. Current concepts of NAFLD pathogenesis describe a “two-hit” model, which includes initial accumulation of triglycerides in hepatocytes due to impaired β-oxidation, followed by secondary inflammatory injury mediated by proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The progression from steatosis to steatohepatitis and cirrhosis is closely related to the functional state of the antioxidant defense system and genetic predisposition.