Glycoxidation: the menace of diabetes and aging

Abstract

Advanced glycation end products (AGE) form via the Maillard reaction in vivo and are also consumed from exogenous sources such as diet and smoking. They alter the structure and function of molecules and increase oxidative stress in biological systems. These consequences promote the pathogenesis of diabetic complications and changes associated with aging, including atherosclerosis, and renal, eye, and neurological disease. Both specific and nonspecific receptor mechanisms mediate these detrimental effects but also participate in the removal and degradation of AGE. AGE toxicity may be averted by promising dietary and pharmacological strategies which are currently being investigated.