NAFLD, the hepatic manifestation of the metabolic syndrome

Since the original demonstration that NAFLD is intimately connected with the components of MetS, a lot of clinical and experimental evidence strengthened the concept that fatty liver and its progression have in general the same origin (insulin- resistance) and same outcome (cardiovascular disease) as originally ascribed to MetS [16]. Also, in the subset of patients without obesity (lean NAFLD), the effectiveness of weight loss and lifestyle intervention suggests that the intrinsic metabolic defects are similar to those observed in the presence of overweight/obesity. As long as effective drugs for NAFLD are not available, the treatment of comorbidities, i.e., the features of MetS, remains the sole possible strategy to reduce the burden of disease, selecting compounds that might also be beneficial for the liver. Timely and aggressive pharmacologic treatment is likely to address simultaneously the cardiovascular risk, progression to diabetes and chronic kidney disease and, hopefully, the risk of end-stage liver disease, and hepatocellular carcinoma.