糖基化终末产物在糖尿病胃肠动力中的作用及其机制

Roles and Mechanisms of Advanced Glycation End Products in Diabetic Gastrointestinal Motility

糖尿病(DM)几乎可影响消化道所有部位,约75%的DM患者伴有胃肠动力障碍。DM胃肠动力障碍的确切机制仍不清楚,其发生系由多因素所致,可能与自主神经病变、平滑肌病变、Cajal间质细胞病变等有关。糖基化终末产物(AGEs)是体内葡萄糖与蛋白质、脂质或核酸等经非酶促反应生成的化合物。DM时的高糖环境可促进AGEs形成,AGEs异常蓄积在DM并发症如DM肾病、DM血管病变的发生、发展中起重要作用,但其与DM胃肠动力障碍的相关性少见报道。本文对AGEs在DM胃肠动力中的作用及其可能机制作一综述。

Diabetes mellitus（ DM）affects almost the whole digestive tract. Approximately 75% of the diabetic patients suffer from gastrointestinal motility disorders. The precise mechanism of diabetic gastrointestinal motility disorders is not fully clear. Its pathogenesis is considered to be multifactorial and related with autonomic neuropathy,smooth muscle myopathy and lesions of interstitial cells of Cajal. Advanced glycation end products（ AGEs ） are derived from the nonenzymatic reaction of glucose with proteins,lipids or nucleic acids in vivo. Hyperglycemia in DM is a favourite for formation of AGEs, and excessive accumulation of AGEs contributes to the complications of DM such as diabetic nephropathy and diabetic vascular lesions. However,the correlation of AGEs with diabetic gastrointestinal motility disorders is seldom reported. In this review article,the roles and possible mechanisms of AGEs in diabetic gastrointestinal motility were summarized.