Simultaneous control of hyperglycemia and oxidative stress normalizes endothelial function in type 1 diabetes
Simultaneous control of hyperglycemia and oxidative stress normalizes endothelial function in type 1 diabetes
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DOI：
10.2337/dc06-2048
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发表时间：
2007-03-01
期刊：
影响因子：
16.2
通讯作者：
Giugliano, Dario
中科院分区：
文献类型：
--
作者：
Ceriello, Antonio;Kumar, Sudhesh;Giugliano, Dario
目的-以前的研究表明，在I型糖尿病中，即使血管内皮功能正常化，内皮功能障碍仍然存在。此外，氧化应激最近已被证明是高血糖症诱导的内皮dysfunction.RESEARCH设计和方法-36 1型糖尿病患者和12名对照组的介质。将糖尿病患者分为三组。第一组用胰岛素治疗24小时，达到接近正常化的胰岛素水平。处理12小时后，在剩余的12小时内加入维生素C。第二组用维生素C治疗24 h。在该治疗12小时后，开始胰岛素治疗，在剩余的12小时内达到接近正常化的水平。第三组治疗24小时，维生素C和胰岛素，实现接近正常化的benefit.Results -无论是正常化的benefit. Nor维生素C单独治疗是能够正常化的内皮功能障碍或氧化应激。然而，胰岛素和维生素C的组合正常化endothelial dysfunction和降低氧化应激到正常水平。结论-这项研究表明，I型糖尿病患者的长期高血糖诱导内皮细胞的永久性改变，这可能有助于内皮功能障碍，增加氧化应激，即使高血糖是正常的。
OBJECTIVE - Previous studies have shown that in type I diabetes endothelial dysfunction persists even when glycemia is normalized. Moreover, oxidative stress has recently been demonstrated to be the mediator of hyperglycemia-induced endothelial dysfunction.RESEARCH DESIGN AND METHODS - Thirty-six type 1 diabetic patients and 12 control subjects were enrolled. The diabetic patients were divided into three groups. The first group was treated for 24 h with insulin, achieving a near-normalization of glycemia. After 12 h of this treatment, vitamin C was added for the remaining 12 h. The second group was treated for 24 h with vitamin C. After 12 h of this treatment, insulin was started, with achievement of near-normalization of glycemia for the remaining 12 h. The third group was treated for 24 h with both vitamin C and insulin, achieving near-normalization of glycemia.RESULTS - Neither normalization of glycemia nor vitamin C treatment alone was able to normalize endothelial dysfunction or oxidative stress. However, a combination of insulin and vitamin C normalized enclothelial dysfunction and decreased oxidative stress to normal levels.CONCLUSIONS - This study suggests that long-lasting hyperglycemia in type I diabetic patients induces permanent alterations in endothelial cells, which may contribute to endothelial dysfunction by increased oxidative stress even when hyperglycemia is normalized.