Advanced glycation end-products and the progress of diabetic vascular complications.
Epidemiological studies have confirmed that hyperglycemia is the most important factor in the onset and progress of vascular complications, both in Type 1 and 2 diabetes mellitus. The formation of advanced glycation end-products (AGEs) correlates with glycemic control. The AGE hypothesis proposes that accelerated chemical modification of proteins by glucose during hyperglycemia contributes to the pathogenesis of diabetic complications including nephropathy, retinopathy, neuropathy and atherosclerosis. Recent studies have shown that increased formation of serum AGEs exists in diabetic children and adolescents with or without vascular complications. Furthermore, the presence of diabetic complications in children correlates with elevated serum AGEs. The level of serum AGEs could be considered as a marker of later developments of vascular complications in children with Type 1 and 2 diabetes mellitus. The careful metabolic monitoring of young diabetics together with monitoring of serum AGEs can provide useful information about impending AGE-related diabetic complications. It is becoming clear that anti-AGE strategies may play an important role in the treatment of young and older diabetic patients. Several potential drug candidates such as AGE inhibitors have been reported recently.
Jakus
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Institute of Medical Chemistry, Biochemistry and Clinical Biochemistry, Faculty of Medicine, Comenius University, Sasinkova 2, 811 08 Bratislava, Slovak Republic. jakus@post.sk
Rietbrock
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D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000097:blood / Q000378:metabolism / Q000502:physiology*; D006031:Glycosylation; D006146:Guanidines / Q000627:therapeutic use; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology; D010455:Peptides / Q000378:metabolism; D011733:Pyridoxamine / Q000627:therapeutic use; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000502:physiology; D014652:Vascular Diseases / Q000188:drug therapy / Q000209:etiology*
D017127:Glycation End Products, Advanced; D006146:Guanidines; D010455:Peptides; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D011733:Pyridoxamine; C004479:pimagedine