astaxanthine and Fatty-Liver

Non-alcoholic fatty liver disease (NAFLD) is a common clinicopathological condition, encompassing a range of conditions caused by lipid deposition within liver cells. To date, no approved drugs are available for the treatment of NAFLD, despite the fact that it represents a serious and growing clinical problem in the Western world. Identification of the molecular mechanisms leading to NAFLD-related fat accumulation, mitochondrial dysfunction and oxidative balance impairment facilitates the development of specific interventions aimed at preventing the progression of hepatic steatosis. In this review, we focus our attention on the role of dysfunctions in mitochondrial bioenergetics in the pathogenesis of fatty liver. Major data from the literature about the mitochondrial targeting of some antioxidant molecules as a potential treatment for hepatic steatosis are described and critically analysed. There is ample evidence of the positive effects of several classes of antioxidants, such as polyphenols (

Topics: Animals; Anthocyanins; Antioxidants; Carotenoids; Catechin; Coumestrol; Curcumin; Energy Metabolism; Fatty Liver; Glucosinolates; Humans; Imidoesters; Isothiocyanates; Lipogenesis; Mitochondria; Non-alcoholic Fatty Liver Disease; Nutritional Sciences; Oxidative Stress; Oximes; Polyphenols; Quercetin; Resveratrol; Stilbenes; Sulfoxides; Xanthophylls

Owing to the worldwide epidemic of obesity, and the popularity of diets rich in sugar and saturated fat, nonalcoholic fatty liver disease (NAFLD) is increasingly common; it is usually associated with insulin resistance, and may be considered a component of the metabolic syndrome. The pathologies which can complicate hepatic steatosis--steatohepatitis, cirrhosis, and hepatic cancer--appear to result from an interaction of hepatic lipid overload and hepatic oxidative stress. It is therefore proposed that comprehensive regimens which effectively target each of these precipitating factors should achieve the best therapeutic benefit in NAFLD. Appropriate weight loss, and a diet low in saturated fat, glycemic index, and added sugars, should decrease hepatic lipid load. Measures which enhance adipocyte insulin sensitivity--such as pioglitazone, astaxanthin, and spirulina--may also be helpful in this regard, as may agents that boost hepatocyte capacity for fatty acid oxidation, such as metformin, carnitine, hydroxycitrate, long-chain omega-3 fats, and glycine. Astaxanthin and spirulina appear to have considerable potential for controlling the oxidative stress associated with NAFLD - the former because it may help to prevent the mitochondrial damage that renders mitochondria a key source of superoxide in this syndrome, the latter because it is exceptionally rich in phycocyanobilin, a phytochemical inhibitor of NAPDH oxidase. Other antioxidants which show some promise in this syndrome include high-dose folate, lipoic acid, melatonin, N-acetylcysteine, vitamin E, and taurine. Finally, treatment with salsalate, an inhibitor of IkappaB kinase-beta, has potential for blunting the adverse impact of hepatic steatosis on oxidative stress and inflammation.

Topics: Antioxidants; Fatty Liver; Humans; Oxidative Stress; Salicylates; Xanthophylls