Hypoglycemic Drugs and Advanced Glycation Endproducts

Advanced glycation endproducts and the kidney.

Advanced glycation end products (AGEs) are a heterogeneous group of protein and lipids to which sugar residues are covalently bound. AGE formation is increased in situations with hyperglycemia (e.g., diabetes mellitus) and is also stimulated by oxidative stress, for example in uremia. It appears that activation of the renin-angiotensin system may contribute to AGE formation through various mech...

Novel inhibitors of advanced glycation endproducts.

Enhanced formation and accumulation of advanced glycation endproducts (AGE's) have been proposed to play a major role in the pathogenesis of diabetic complications, aging, atherosclerosis, and Alzheimer disease leading to progressive and irreversible intermolecular protein crosslinkings. This process is accelerated in diabetes and has been postulated to contribute to the development of a range ...

Aging: Drugs to Eliminate Methylglyoxal, a Reactive Glucose Metabolite, and Advanced Glycation Endproducts

Advanced glycation endproducts and plaque instability: a link beyond diabetes.

Despite clear advances in the treatment of vascular disease, we are still far from the understanding and valid assessment of the natural history of atherosclerotic plaque. Several studies have shown that the vulnerable plaque is the main culprit for ischaemic cardiac and cerebral events, but reliable indicators of plaque instability remain elusive in clinical practice. This aspect deserves atte...

Advanced Glycation Endproducts Interfere with Adhesion and Neurite Outgrowth

Advanced glycation endproducts (AGEs) represent a non-enzymatic posttranslational protein modification. AGEs are generated by a series of chemical reactions of free reducing monosaccharides, such as glucose, fructose or metabolites of the monosaccharide metabolism with amino groups of proteins. After oxidation, dehydration and condensation, stable AGE-modifications are formed. AGE-modified prot...