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Epigenetic Mechanisms Underlying the Link between Non-Alcoholic Fatty Liver Diseases and Nutrition

Lee, Joo Ho, Friso, Simonetta, Choi, Sang-Woon
Nutrients 2014 v.6 no.8 pp. 3303-3325
DNA, DNA methylation, alcohols, biochemical pathways, disease course, epigenetics, fatty liver, gene expression, hepatocytes, hepatoma, histones, hyperlipidemia, hypertension, inflammation, inheritance (genetics), insulin resistance, liver, metabolic syndrome, metabolism, microRNA, nucleotide sequences, nutrition, obesity, oxidative stress, pathogenesis, patients, therapeutics, triacylglycerols
Non-alcoholic fatty liver disease (NAFLD) is defined as a pathologic accumulation of fat in the form of triglycerides (TG) in the liver (steatosis) that is not caused by alcohol. A subgroup of NAFLD patients shows liver cell injury and inflammation coupled with the excessive fat accumulation (steatohepatitis), which is referred to as non-alcoholic steatohepatitis (NASH). Patients with NASH may develop cirrhosis and hepatocellular carcinoma (HCC). NAFLD shares the key features of metabolic syndrome including obesity, hyperlipidemia, hypertension, and insulin resistance. The pathogenesis of NAFLD is multi-factorial, however the oxidative stress seems to plays a major role in the development and progression of the disease. The emerging field of epigenetics provides a new perspective on the pathogenesis of NAFLD. Epigenetics is an inheritable but reversible phenomenon that affects gene expression without altering the DNA sequence and refers to DNA methylation, histone modifications and microRNAs. Epigenetic manipulation through metabolic pathways such as one-carbon metabolism has been proposed as a promising approach to retard the progression of NAFLD. Investigating the epigenetic modifiers in NAFLD may also lead to the development of preventive or therapeutic strategies for NASH-associated complications.