'Toxicity of glucose: is AGE the answer?'.
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.
Makita
Z
Z
Internal Medicine II, Hokkaido University, School of Medicine, Sapporo, Japan.
D000818:Animals; D003928:Diabetic Nephropathies / Q000150:complications / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006031:Glycosylation; D006801:Humans; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000378:metabolism*; D010455:Peptides / Q000378:metabolism
D010455:Peptides; D005947:Glucose