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首页> 外文期刊>The Journal of Nutritional Biochemistry >Alpha-lipoic acid improves high-fat diet-induced hepatic steatosis by modulating the transcription factors SREBP-1, FoxO1 and Nrf2 via the SIRT1/LKB1/AMPK pathway
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Alpha-lipoic acid improves high-fat diet-induced hepatic steatosis by modulating the transcription factors SREBP-1, FoxO1 and Nrf2 via the SIRT1/LKB1/AMPK pathway

机译：α-硫辛酸通过SIRT1 / LKB1 / AMPK途径调节转录因子SREBP-1，FoxO1和Nrf2改善高脂饮食诱导的肝脂肪变性

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Understanding the mechanism by which alpha-lipoic acid supplementation has a protective effect upon nonalcoholic fatty liver disease in vivo and in vitro may lead to targets for preventing hepatic steatosis. Male C57BL/6J mice were fed a normal diet, high-fat diet or high-fat diet supplemented with alpha-lipoic acid for 24 weeks. HepG2 cells were incubated with normal medium, palmitate or alpha-lipoic acid. The lipid-lowering effects were measured. The protein expression and distribution were analyzed by Western blot, immunoprecipitation and immunofluorescence, respectively. We found that alpha-lipoic acid enhanced sirtuin 1 deacetylase activity through liver kinase B1 and stimulated AMP-activated protein kinase. By activating the sirtuin 1/liver kinase B1/AMP-activated protein kinase pathway, the translocation of sterol regulatory element-binding protein-1 into the nucleus and forkhead box O1 into the cytoplasm was prevented. Alpha-lipoic acid increased adipose triacylglycerol lipase expression and decreased fatty acid synthase abundance. In in vivo and in vitro studies, alpha-lipoic acid also increased nuclear NF-E2-related factor 2 levels and downstream target amounts via the sirtuin 1 pathway. Alpha-lipoic acid eventually reduced intrahepatic and serum triglyceride content. The protective effects of alpha-lipoic acid on hepatic steatosis appear to be associated with the transcription factors sterol regulatory element-binding protein-1, forkhead box O1 and NF-E2-related factor 2. (C) 2014 The Authors. Published by Elsevier Inc.
机译：了解体内和体外补充α-硫辛酸对非酒精性脂肪肝具有保护作用的机制可能会导致预防肝脂肪变性的靶标。给雄性C57BL / 6J小鼠喂食正常饮食，高脂饮食或补充α-硫辛酸的高脂饮食24周。将HepG2细胞与正常培养基，棕榈酸酯或α-硫辛酸孵育。测量了降脂作用。通过蛋白质印迹，免疫沉淀和免疫荧光分别分析蛋白质的表达和分布。我们发现，α-硫辛酸可通过肝脏激酶B1增强sirtuin 1脱乙酰酶活性，并刺激AMP激活的蛋白激酶。通过激活sirtuin 1 /肝激酶B1 / AMP激活的蛋白激酶途径，可以防止固醇调节元件结合蛋白-1转运到细胞核中，而叉头盒O1转运到细胞质中。 α-硫辛酸增加脂肪三酰基甘油脂肪酶的表达并降低脂肪酸合酶的丰度。在体内和体外研究中，α-硫辛酸还通过Sirtuin 1途径增加了核NF-E2相关因子2水平和下游目标量。硫辛酸最终降低了肝内和血清甘油三酯的含量。 α-硫辛酸对肝脂肪变性的保护作用似乎与转录因子固醇调节元件结合蛋白-1，叉头盒O1和NF-E2相关因子2有关。（C）2014作者。由Elsevier Inc.发布

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