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糖基化的负面后果。

Negative consequences of glycation.

作者信息

Brownlee M

机构信息

Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

出版信息

Metabolism. 2000 Feb;49(2 Suppl 1):9-13. doi: 10.1016/s0026-0495(00)80078-5.

DOI:10.1016/s0026-0495(00)80078-5
PMID:10693913
Abstract

The Diabetes Control and Complications Trial (DCCT) established unequivocally that the effects of inadequate insulin action (as monitored by the level of hyperglycemia) are associated with the incidence and progression of diabetic retinopathy, nephropathy, and neuropathy. How does hyperglycemia induce the functional and morphologic changes that characterize diabetic complications? Increasing evidence points to a major role for sugar-derived advanced glycation end products (AGEs), which form inside and outside cells as a function of glucose concentration. Recent work in this area supports a central role for reactive oxygen species (ROS) in both the formation of AGEs, and in AGE-induced pathologic alterations in gene expression. Inhibition of ROS may also be centrally important in the action of drugs that prevent complications in diabetic animal models.

摘要

糖尿病控制与并发症试验(DCCT)明确证实,胰岛素作用不足(通过高血糖水平监测)的影响与糖尿病视网膜病变、肾病和神经病变的发生及进展相关。高血糖是如何引发具有糖尿病并发症特征的功能和形态学变化的呢?越来越多的证据表明,糖衍生的晚期糖基化终产物(AGEs)起着主要作用,其在细胞内外的形成是葡萄糖浓度的函数。该领域的最新研究支持活性氧(ROS)在AGEs形成以及AGE诱导的基因表达病理改变中都发挥着核心作用。在预防糖尿病动物模型并发症的药物作用中,抑制ROS可能也至关重要。

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