Non-alcoholic fatty liver disease (NAFLD) is characterized by excess lipids in hepatocytes,\ndue to excessive fatty acid influx from adipose tissue, de novo hepatic lipogenesis, in addition to\nexcessive dietary fat and carbohydrate intake. Chronic hepatic lipid overload induces mitochondrial\noxidative stress and cellular damage leading the development of NAFLD into a more severe liver\ndisease condition, non-alcoholic steato-hepatitis (NASH). In turn, this can progress to cirrhosis and\nhepatocellular carcinoma (HCC). Among others, copper is one of the main bio-metals required for\nthe preponderance of the enzymes involved in physiological redox reactions, which primarily occurs\nduring mitochondrial respiration. Thus, copper homeostasis could be considered a target point for\ncounteracting the progression of NAFLD. Accordingly, many diseases are correlated to unbalanced\ncopper levels and, actually, some clinical trials are examining the use of copper chelating agents.\nCurrently, no pharmacological interventions are approved for NAFLD, but nutritional and lifestyle\nmodifications are always recommended. Fittingly, antioxidant food agents recognized to improve\nNAFLD and its complications have been described in the literature to bind copper. Therefore, this\nreview describes the role of nutrition in the development and progression of NAFLD with a particular\nfocus on copper and copper-binding antioxidant compounds against NAFLD.
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