Background: Fatty liver, or steatosis, is a condition of excess accumulation of lipids, mainly
under form of triglycerides (TG), in the liver, and it is the hallmark of non-alcoholic fatty liver disease
(NAFLD). NAFLD is the most common liver disorder world-wide and it has frequently been associated
with obesity, hyperlipidemia and insulin resistance. Free fatty acids (FA) are the major mediators of hepatic
steatosis; patients with NAFLD have elevated levels of circulating FA that correlate with disease
Methods: Steatosis is a reversible condition that can be resolved with changed behaviors, or that can
progress towards more severe liver damages such as steatohepatitis (NASH), fibrosis and cirrhosis. In
NAFLD, FA of exogenous or endogenous origin accumulate in the hepatocytes and trigger liver damages.
Excess TG are stored in cytosolic lipid droplets (LDs) that are dynamic organelles acting as hubs
for lipid metabolism.
Results: In the first part of this review, we briefly reassumed the main classes of FA and their chemical
classification as a function of the presence and number of double bonds, their metabolic pathways and
effects on human health. Then, we summarized the main genetic and diet-induced animal models of
NAFLD, as well as the cellular models of NAFLD.
Conclusions: In recent years, both the diet-induced animal models of NAFLD as well as the cellular
models of NAFLD have found ever more application to investigate the mechanisms involved in
NAFLD, and we referred to their advantages and disadvantages.