An Intimate Relationship between ROS and Insulin Signalling: Implications for Antioxidant Treatment of Fatty Liver Disease.
An Intimate Relationship between ROS and Insulin Signalling: Implications for Antioxidant Treatment of Fatty Liver Disease.
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DOI：
10.1155/2014/519153
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发表时间：
2014
影响因子：
--
通讯作者：
Estall JL
中科院分区：
文献类型：
--
作者：
Besse-Patin A;Estall JL
氧化应激会损害多种细胞成分，包括 DNA、脂质和蛋白质，并与非酒精性脂肪肝 (NAFLD) 的病理改变有关。由营养超载和线粒体功能障碍引起的活性氧 (ROS) 排放被认为是 NAFLD 进展的主要介质，特别是肝脏胰岛素抵抗的发展。在胰岛素信号传导的背景下，ROS 具有双重作用，既是胰岛素信号级联的促进剂又是抑制剂。 ROS 通过影响磷酸酶活性、应激敏感激酶和代谢传感器的半胱氨酸残基的氧化还原修饰来介导这些效应。这篇综述强调了脂肪肝疾病中氧化还原敏感蛋白和胰岛素信号传导之间的复杂关系，以及在更大程度上强调了活性氧作为代谢活跃细胞中主要信号传导分子的重要性。
Oxidative stress damages multiple cellular components including DNA, lipids, and proteins and has been linked to pathological alterations in nonalcoholic fatty liver disease (NAFLD). Reactive oxygen species (ROS) emission, resulting from nutrient overload and mitochondrial dysfunction, is thought to be a principal mediator in NAFLD progression, particularly toward the development of hepatic insulin resistance. In the context of insulin signalling, ROS has a dual role, as both a facilitator and inhibitor of the insulin signalling cascade. ROS mediate these effects through redox modifications of cysteine residues affecting phosphatase enzyme activity, stress-sensitive kinases, and metabolic sensors. This review highlights the intricate relationship between redox-sensitive proteins and insulin signalling in the context of fatty liver disease, and to a larger extent, the importance of reactive oxygen species as primary signalling molecules in metabolically active cells.