Volume 70 Number 4 September 2003	back to contents

¹Professor, Department of Geriatrics, Division of Experimental Diabetes and Aging, and ²Clinical Fellow, Department of Medicine, Division of Endocrinology, Mount Sinai School of Medicine, New York, NY.

Address all correspondence to Helen Vlassara, M.D., Director, Division of Experimental Diabetes and Aging, Box 1640,
Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029; Email: helen.vlassara@mssm.edu.

Adapted from a Grand Rounds presentation to the Department of Medicine, Mount Sinai School of Medicine, New York, NY on November 6, 2001 and updated as of January 2003.

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.

KEY WORD

Glycoxidation, advanced glycation end product, oxidative stress, macroangiopathy, microangiopathy.

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