Objective: To review the literature on the advanced glycation end products (AGEs) in diabetes, with especial interest on their role in the pathophysiology of the chronic complications of diabetes mellitus.
Materials: Representative papers were selected through a computer MEDLINE search from 1985 to 2000.
Results: Hyperglycemia causes irreversible microvascular and macrovascular complications, including retinopathy, neuropathy, nephropathy, atherosclerosis and cerebrovascular disease. There is evidence that glycation leads to chemical modification of proteins, and other macromolecules and it contributes to the pathogenesis of diabetic complications. Several AGEs and their receptors have been identified. The inhibition of AGE formation is under intensive investigation to prevent diabetic complications. From several inhibitors studied, Amadorins offer great therapeutic potential.
Conclusions: It is known that a heterogeneous group of AGEs is formed by glycation. The mechanism of AGE formation is partially understood, making it difficult to identify the precise chemical products responsible for in vivo damage and also to develop specific inhibitors.