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Curr Med Chem. 2017 May 17. doi: 10.2174/0929867324666170518101334. [Epub ahead of print]

Fatty acids and effects on in vitro and in vivo models of liver steatosis.

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1
DISTAV, UniversitĂ  di Genova, Corso Europa 26, 16132 Genova . Italy.

Abstract

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 severity. 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. 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, that have found ever more application in recent years to investigate the mechanisms involved in NAFLD, also referring to their advantages and disadvantages.

KEYWORDS:

fatty acid oxidation; fatty acids; hepatic steatosis; lipid droplets (LDs); lipid metabolism; nonalcoholic fatty liver disease (NAFLD); oxidative stress; reactive oxygen species (ROS)

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