Vlassara Helen, Palace Marcia Rashelle
Division of Experimental Diabetes and Aging, Box 1640, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA.
Mt Sinai J Med. 2003 Sep;70(4):232-41.
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.
晚期糖基化终末产物（AGE）在体内通过美拉德反应形成，也可从饮食和吸烟等外源性来源摄入。它们会改变分子的结构和功能，并增加生物系统中的氧化应激。这些后果会促进糖尿病并发症的发病机制以及与衰老相关的变化，包括动脉粥样硬化、肾脏、眼睛和神经疾病。特异性和非特异性受体机制介导了这些有害作用，但也参与了AGE的清除和降解。目前正在研究的有前景的饮食和药理学策略可能会避免AGE的毒性。
