Hypoxia, Oxidative Stress and Fat.
Hypoxia, Oxidative Stress and Fat.
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DOI：
10.3390/biom5021143
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发表时间：
2015-06-08
期刊：
影响因子：
5.5
通讯作者：
Pesta D
中科院分区：
文献类型：
--
作者：
Netzer N;Gatterer H;Faulhaber M;Burtscher M;Pramsohler S;Pesta D
肥胖个体的白色脂肪组织中的代谢紊乱有助于胰岛素抵抗的发病机制和2型糖尿病的发展。脂肪细胞中胰岛素作用受损与脂解升高和游离脂肪酸增加相关，导致肝脏和骨骼肌中异位脂肪沉积。慢性脂肪组织缺氧已被认为是导致脂肪细胞功能障碍的病理机制的一部分。缺氧可引起人和动物脂肪细胞的氧化应激，并减少有益脂肪因子如脂联素的产生。然而，缺氧的时间-剂量反应使缺氧应激的作用相对化。脂肪细胞长期暴露在缺氧环境中会导致有益物质的产生，如瘦素。关于缺氧对白色脂肪组织的时间-剂量反应以及脂肪细胞中氧化应激产生的时间过程的知识仍然很少。本文综述了脂肪组织缺氧，氧化应激，线粒体功能障碍，脂肪细胞肥大，巨噬细胞浸润和炎症介质的产生引起的低度炎症之间的潜在联系。
Metabolic disturbances in white adipose tissue in obese individuals contribute to the pathogenesis of insulin resistance and the development of type 2 diabetes mellitus. Impaired insulin action in adipocytes is associated with elevated lipolysis and increased free fatty acids leading to ectopic fat deposition in liver and skeletal muscle. Chronic adipose tissue hypoxia has been suggested to be part of pathomechanisms causing dysfunction of adipocytes. Hypoxia can provoke oxidative stress in human and animal adipocytes and reduce the production of beneficial adipokines, such as adiponectin. However, time-dose responses to hypoxia relativize the effects of hypoxic stress. Long-term exposure of fat cells to hypoxia can lead to the production of beneficial substances such as leptin. Knowledge of time-dose responses of hypoxia on white adipose tissue and the time course of generation of oxidative stress in adipocytes is still scarce. This paper reviews the potential links between adipose tissue hypoxia, oxidative stress, mitochondrial dysfunction, and low-grade inflammation caused by adipocyte hypertrophy, macrophage infiltration and production of inflammatory mediators.