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Advanced Glycoxidation End-Products Advanced Glycoxidation End-Products Advanced Glycoxidation End-Products Advanced Glycoxidation End-Products

Microangiopathy Advanced Glycoxidation End-Products and Diabetic

Macroangiopathy Antiadvanced Glycoxidation End-Product Strategies Conclusions References introduction

The incidence of diabetes, especially type 2 diabetes, is increasing at an alarming rate assuming epidemic proportions (1). Worldwide, 124 million people had diabetes by 1997, although an estimated 221 million people will have diabetes by the year 2010 (1).

Diabetic patients may suffer a number of debilitating complications such as retinopa-thy, nephropathy, neuropathy, and atherosclerosis resulting in cardiovascular, cere-brovascular, or peripheral vascular disease. These diabetic complications lead to huge economic and psychosocial consequences. Although the pathogenesis of type 1 diabetes is different from that of type 2 diabetes, the pathophysiology of vascular complications in the two conditions appears to be similar.

Two landmark clinical studies, the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study, showed that intensive control of hyperglycemia could reduce the occurrence or progression of retinopathy, neuropathy and nephropathy in patients with type 1 and type 2 diabetes (2,3). Although these studies reinforce the important role of hyperglycemia in the pathogenesis of diabetic complica-

From: Contemporary Cardiology: Diabetes and Cardiovascular Disease, Second Edition Edited by: M. T. Johnstone and A. Veves © Humana Press Inc., Totowa, NJ

Metabolism Interactions and Diabetic tions, the identification of the mechanisms by which hyperglycemia exerts these effects remains limited (4).

It is well known that long-term hyperglycemia leads to the formation of advanced glycation or glycoxidation end-products (AGEs), which mediate most of the deleterious effects of hyperglycemia and seem to play a significant role in the pathogenesis of diabetic complications (5,6). AGEs, together with the interrelated processes of oxidative stress and inflammation, may account for many of the complications of diabetes (5,6). Evidence for this emerges not only from an increased number of in vitro and in vivo studies exploring the role of AGEs in different pathologies, but also from studies demonstrating significant improvement of features of diabetic complications by inhibitors of the glycoxidation process (7-13).

In the following review we will provide a general overview of the nature, formation, and action of AGEs and recent evidence on their pathogenic potential in the initiation and progression of diabetic complications. We will conclude delineating possible therapeutic interventions based on this new knowledge.

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