Department of Pediatrics, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Free Radic Biol Med. 2011 Mar 1;50(5):567-75. doi: 10.1016/j.freeradbiomed.2010.12.006. Epub 2010 Dec 13.
Oxidative stress has been implicated as a contributor to both the onset and the progression of diabetes and its associated complications. Some of the consequences of an oxidative environment are the development of insulin resistance, β-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction, which can lead ultimately to the diabetic disease state. Experimental and clinical data suggest an inverse association between insulin sensitivity and ROS levels. Oxidative stress can arise from a number of different sources, whether disease state or lifestyle, including episodes of ketosis, sleep restriction, and excessive nutrient intake. Oxidative stress activates a series of stress pathways involving a family of serine/threonine kinases, which in turn have a negative effect on insulin signaling. More experimental evidence is needed to pinpoint the mechanisms contributing to insulin resistance in both type 1 diabetics and nondiabetic individuals. Oxidative stress can be reduced by controlling hyperglycemia and calorie intake. Overall, this review outlines various mechanisms that lead to the development of oxidative stress. Intervention and therapy that alter or disrupt these mechanisms may serve to reduce the risk of insulin resistance and the development of diabetes.
氧化应激被认为是导致糖尿病及其相关并发症发生和进展的一个因素。氧化环境的一些后果包括胰岛素抵抗、β细胞功能障碍、葡萄糖耐量受损和线粒体功能障碍，最终导致糖尿病状态。实验和临床数据表明，胰岛素敏感性与 ROS 水平之间存在反比关系。氧化应激可能来自许多不同的来源，无论是疾病状态还是生活方式，包括酮症发作、睡眠限制和过量营养摄入。氧化应激激活了一系列涉及丝氨酸/苏氨酸激酶家族的应激途径，这反过来又对胰岛素信号产生负面影响。需要更多的实验证据来确定导致 1 型糖尿病患者和非糖尿病患者胰岛素抵抗的机制。通过控制高血糖和热量摄入可以减少氧化应激。总的来说，这篇综述概述了导致氧化应激发展的各种机制。改变或破坏这些机制的干预和治疗可能有助于降低胰岛素抵抗和糖尿病的风险。
