Méndez José D
Unidad de Investigación Médica en Enfermedades Metabólicas, 4o. Piso. Hospital de Especialidades, Centro Médico Nacional SXXI, IMSS.
Gac Med Mex. 2003 Jan-Feb;139(1):49-55.
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.
Representative papers were selected through a computer MEDLINE search from 1985 to 2000.
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.
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.
回顾有关糖尿病中晚期糖基化终末产物(AGEs)的文献,特别关注其在糖尿病慢性并发症病理生理学中的作用。
通过计算机检索MEDLINE数据库,选取1985年至2000年期间的代表性论文。
高血糖会引发不可逆的微血管和大血管并发症,包括视网膜病变、神经病变、肾病、动脉粥样硬化和脑血管疾病。有证据表明糖基化会导致蛋白质及其他大分子发生化学修饰,进而促使糖尿病并发症的发病机制。已鉴定出多种AGEs及其受体。目前正在深入研究抑制AGE形成以预防糖尿病并发症。在所研究的几种抑制剂中,氨基胍具有巨大的治疗潜力。
已知糖基化会形成一组异质性的AGEs。AGE形成的机制部分已明,这使得难以确定体内损伤的确切化学产物,也难以开发出特异性抑制剂。