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Role of adipokines and peroxisome proliferator-activated receptors in nonalcoholic fatty liver disease

查看全文 作  者:Vettickattuparambil George [1]Giby;Thekkuttuparambil Ananthanarayanan [1]Ajith 高影响力作者 机构地区:[1]Department of Biochemistry, Amala Institute of Medical Sciences, Thrissur-680 555, Kerala, India高影响力机构 出  处:《World Journal of Hepatology》索引2014年第6卷第8期,共10页高影响力期刊 摘  要:Intrahepatic fat deposition has been demonstrated in patients with nonalcoholic fatty liver disease(NAFLD). Genetic and environmental factors are important for the development of NAFLD. Diseases such as obesity, diabetes, and hypertension have been found to be closely associated with the incidence of NAFLD. Evi-dence suggests that obesity and insulin resistance are the major factors that contribute to the development of NAFLD. In comparing the factors that contribute to the buildup of excess calories in obesity, an imbalance of energy homeostasis can be considered as the basis. Among the peripheral signals that are generated to regulate the uptake of food, signals from adipose tissue are of major relevance and involve the maintenance of energy homeostasis through processes such as lipo-genesis, lipolysis, and oxidation of fatty acids. Advances in research on adipose tissue suggest an integral role played by adipokines in NAFLD. Cytokines secreted by adipocytes, such as tumor necrosis factor-α, transform-ing growth factor-β, and interleukin-6, are implicated in NAFLD. Other adipokines, such as leptin and adiponectin and, to a lesser extent, resistin and retinol binding protein-4 are also involved. Leptin and adiponectin can augment the oxidation of fatty acid in liver by activating the nuclear receptor super-family of transcription fac-tors, namely peroxisome proliferator-activated receptor(PPAR)-α. Recent studies have proposed downregula-tion of PPAR-α in cases of hepatic steatosis. This re-view discusses the role of adipokines and PPARs with regard to hepatic energy metabolism and progression of NAFLD. 关 键 词:NONALCOHOLIC FATTY liver disease ADIPOSE tissue Energy HOMEOSTASIS PEROXISOME proliferator activated receptors ADIPOKINES
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