IntroductionThe hallmark of nonalcoholic fatty liver disease (NAFLD) is the intrahepatocyte accumulation of lipids with or without necro-inflammatory changes and ballooning [i.e., steatohepatitis or nonalcoholic steatohepatitis (NASH)], fibrosis, cirrhosis and hepatocellular carcinoma (HCC), which is observed in dysmetabolic individuals in the absence of competing causes of chronic liver disease such as excess alcohol consumption, viral infections, autoimmune or hereditary conditions and steatogenic medications (1). NAFLD represents an example of lipotoxicity caused by ectopic lipid accumulation. Even relatively modest amounts of ectopic lipid accumulation in normally lean organs (e.g., liver, pancreas, heart, kidney and muscle) can trigger functional disturbance in the affected organs and a subsequent vicious circle of adverse metabolic consequences in predisposed individuals (1); this will eventually result in those hepatic and extra-hepatic manifestations and co-morbid conditions which are frequently observed in NAFLD patients. Under this perspective, NAFLD should be viewed as one of the systemic manifestations and consequences resulting from lipid overflow.