Reducing oxidative stress in patients with type 2 diabetes mellitus: A primary care call to action

Jeff Unger MD
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引用次数: 32

Abstract

Background: Oxidative stress is believed to be the primary cause of the microvascular and macrovascular complications of type 2 diabetes mellitus (DM).

Objective: This paper examines the evidence linking oxidative stress with long-term complications of type 2 DM and explores methods to minimize its effect.

Methods: A literature search was performed to identify relevant studies for this review. Articles published in English from 2000 to 2008 were identified through searches of PubMed, Diabetes Care, and Google using the search terms oxidative stress, postprandial hyperglycemia, ACCORD Trial, and endothelial cell dysfunction.

Results: The literature search identified 423 articles. Although chronic hyperglycemia can be effectively monitored and targeted using glycosylated hemoglobin concentrations, postprandial glucose levels are also important. Postprandial glucose excursions are exhibited by almost all patients with type 2 DM and are independent risk factors for cardiovascular morbidity and mortality. Furthermore, glucose fluctuations during the postprandial period elicit more oxidative stress than chronic, sustained hyperglycemia and can lead to endothelial dysfunction, vascular inflammation, and microvascular complications. In turn, endothelial dysfunction has been implicated in the development of vascular pathologies such as atherosclerosis. Pharmacologic interventions (eg, rapid-acting insulin analogues that target post-prandial glucose excursions) reduce oxidative stress and vascular inflammation and improve endothelial dysfunction.

Conclusions: Given the important role of oxidative stress in the development of complications of type 2 DM, physi-cians should consider methods to reduce oxidative stress that may occur during both acute (postprandial) and chronic hyperglycemia. One critical aspect is to reduce postprandial glucose levels to <180 mg/dL while lowering fasting glucose levels to <110 mg/dL. By coaching patients to reach these goals, physicians and other health care professionals can minimize the risk of long-term complications of type 2 DM.

降低2型糖尿病患者的氧化应激:初级保健的行动呼吁
背景:氧化应激被认为是2型糖尿病(DM)微血管和大血管并发症的主要原因。目的:探讨氧化应激与2型糖尿病长期并发症之间的关系,并探讨降低氧化应激影响的方法。方法:通过文献检索来确定本综述的相关研究。从2000年到2008年发表的英文文章通过PubMed, Diabetes Care和Google的搜索来确定,搜索词包括氧化应激,餐后高血糖,ACCORD试验和内皮细胞功能障碍。结果:检索到文献423篇。虽然慢性高血糖可以通过糖化血红蛋白浓度有效监测和靶向,餐后血糖水平也很重要。几乎所有2型糖尿病患者都表现出餐后血糖升高,这是心血管疾病发病率和死亡率的独立危险因素。此外,餐后期间的血糖波动比慢性持续高血糖引起更多的氧化应激,并可导致内皮功能障碍、血管炎症和微血管并发症。反过来,内皮功能障碍与动脉粥样硬化等血管病变的发展有关。药物干预(如针对餐后血糖升高的速效胰岛素类似物)可减少氧化应激和血管炎症,改善内皮功能障碍。结论:考虑到氧化应激在2型糖尿病并发症发展中的重要作用,医生应考虑降低急性(餐后)和慢性高血糖期间可能发生的氧化应激的方法。一个关键的方面是将餐后血糖水平降低到180毫克/分升,同时将空腹血糖水平降低到110毫克/分升。通过指导患者达到这些目标,医生和其他卫生保健专业人员可以将2型糖尿病长期并发症的风险降至最低。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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