Eriksson Jan W
The Lundberg Laboratory for Diabetes Research, Institute of Medicine, Sahlgrenska University Hospital, SE 41345 Gothenburg, Sweden.
FEBS Lett. 2007 Jul 31;581(19):3734-42. doi: 10.1016/j.febslet.2007.06.044. Epub 2007 Jun 27.
The metabolic syndrome is a cluster of cardiovascular risk factors, and visceral adiposity is a central component that is also strongly associated with insulin resistance. Both visceral obesity and insulin resistance are important risk factors for the development of type 2 diabetes. It is likely that adipose tissue, particularly in the intra-abdominal depot, is part of a complex interplay involving several tissues and that dysregulated hormonal, metabolic and neural signalling within and between organs can trigger development of metabolic disease. One attractive hypothesis is that many factors leading to insulin resistance are mediated via the generation of abnormal amounts of reactive oxygen species (ROS). There is much evidence supporting that detrimental effects of glucose, fatty acids, hormones and cytokines leading to insulin resistance can be exerted via such a common pathway. This review paper mainly focuses on metabolic and other 'stress' factors that affect insulin's target cells, in particular adipocytes, and it will highlight oxidative stress as a potential unifying mechanism by which these stress factors promote insulin resistance and the development and progression of type 2 diabetes.
代谢综合征是一组心血管危险因素，内脏肥胖是其中的核心组成部分，且与胰岛素抵抗也密切相关。内脏肥胖和胰岛素抵抗都是2型糖尿病发生的重要危险因素。脂肪组织，尤其是腹部脂肪库，很可能是涉及多个组织的复杂相互作用的一部分，器官内部和之间激素、代谢及神经信号失调会引发代谢性疾病。一个有吸引力的假说是，许多导致胰岛素抵抗的因素是通过产生异常量的活性氧（ROS）介导的。有大量证据支持，葡萄糖、脂肪酸、激素和细胞因子导致胰岛素抵抗的有害作用可通过这一共同途径发挥。本文主要关注影响胰岛素靶细胞，尤其是脂肪细胞的代谢及其他“应激”因素，并将强调氧化应激作为一种潜在的统一机制，通过该机制这些应激因素促进胰岛素抵抗以及2型糖尿病的发生和发展。
