'Toxicity of glucose: is AGE the answer?'

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Abstract
Despite a growing knowledge of the pathogenesis of diabetic nephropathy, the increased incidence of end-stage renal disease in diabetic patients continue to pose problems of enormous public health and economic importance. Recently, a growing body of evidence has linked the accumulation of the late products of glucose–protein interaction to a variety of chronic complications, including diabetic nephropathy. The formation of irreversible ‘advanced glycosylation endproducts’ resulting from the spontaneous reaction between glucose and proteins occurs most noticeably on long-lived structural proteins. In this article, I review recent studies suggesting that the pathogenesis of diabetic nephropathy leading to end-stage renal disease is caused by the hyperglycaemia-accelerated formation of advanced glycosylation endproducts. Recent studies suggest that reactive AGE peptides in the circulation potentially play a role as a new version of so called ‘middle molecules toxic substances’. The evidence is opening a new window for our understanding of the pathogenesis of diabetic end-stage renal disease and the benefits of various of treatment modalities.