【摘要】 酒精性脂肪肝(AFL)是长期大量饮用酒精引发的肝脏损害性病变,可逆转也可进一步发展为肝纤维化和肝硬化。众多的脂肪细胞因子如瘦素(Leptin)、抵抗素(Resistin)和肿瘤坏死因子-α(TNF-α)在脂肪肝的发病中起到一定的促进作用,脂联素(Adiponectin)能改善脂质代谢,延缓脂肪肝的发生;脂联素通过腺苷酸活化蛋白激酶(AMPK)调节糖脂代谢、改善胰岛素敏感性。脂联素/AMPK信号通路是酒精在肝脏的作用靶点、也是调节PPARγ作用的重要信号通路;脂肪分化相关蛋白(ADRP)调节脂质代谢、促进酒精性脂肪肝的形成;过氧化物酶增殖体激活受体γ(PPARγ)参与机体脂质稳态的调节,脂肪肝时PPARγ表达增高,肝纤维化时PPARγ表达减少。对酒精性脂肪肝脂质代谢的深入研究,有助于阐明酒精性脂肪肝发病机制并为临床防治ALD及脂质代谢相关疾病提供新策略。更多还原

【Abstract】 Alcoholic fatty liver(AFL) is reversible condition,but it can potentiate the development of alcoholic hepatitis and even cirrhosis if alcohol consumption is continued.Many adipocytokines such as leptin,resistin and TNF-α have an important relationship with hepatic steatosis,while adiponectin has protective effect on AFL.Adiponectin confers protection against alcoholic fatty liver via modulation of AMP-activated protein kinase(AMPK).Adiponectin-AMPK is the key signal transduction pathway involved in the action of PPARγ agonist protection against alcoholic fatty liver.Adipose differentiation-related protein(ADRP) could regulate lipid metabolism and aggravate the formation of AFL.Overexpression of peroxisome proliferator-activated receptor γ(PPAR γ) may cause a serious lipid metabolic disturbance.Whereas expression of PPARγ is markedly high in alcoholic fatty liver,expression of PPARγ in alcoholic hepatic fibrosis is obviously low.This article discussed the mechanisms by which alcohol contributes to increasing lipid accumulation in the liver;further elucidation of these findings would provide a novel therapeutic strategy for treating alcoholic liver disease and other lipid metabolism-related diseases.更多还原