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Glycation and Glycoxidation in Diabetic Vascular Disease

  • Chapter
Oxidative Stress and Vascular Disease

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 224))

Abstract

Elevated blood sugar is the hallmark of diabetes. Paradoxically, increased blood glucose occurs both when there is a complete absence of insulin in the body (type I, insulin dependent diabetes mellitus (IDDM)) and when there is an excess of circulating insulin (type II, non-insulin dependent diabetes mellitus (NIDDM)). Type I diabetes is generally associated with a young or juvenile onset, while Type II diabetes typically occurs with older age and obesity. However, individuals affected by either type of diabetes are at risk for developing a similar set of chronic complications. Microvascular disease in diabetes includes retinopathy, nephropathy and neuropathy. Macrovascular disease is associated with the 2–4 fold increased risk for atherosclerosis and ischemic heart disease observed in diabetic individuals. An unexpected finding in diabetes is that the tissues and cells in which complications occur, such as retinal and other vascular endothelial cells, renal mesangial cells and neural cells do not require insulin for glucose uptake. Because of the common occurrence of elevated circulating glucose, overlap in the complications associated with both type of diabetes, and development of complications in tissues freely permeable to glucose, much research has focused on mechanisms by which glucose itself may contribute to vascular disease in diabetes.

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© 2000 Springer Science+Business Media New York

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Thorpe, S.R., Lyons, T.J., Baynes, J.W. (2000). Glycation and Glycoxidation in Diabetic Vascular Disease. In: Keaney, J.F. (eds) Oxidative Stress and Vascular Disease. Developments in Cardiovascular Medicine, vol 224. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4649-8_14

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