食源性晚期糖基化终末产物与非酒精性脂肪肝关系的研究进展

Research Progress in Relationship between Dietary Advanced Glycation End Products and Nonalcoholic Fatty Liver Disease

非酒精性脂肪肝(NAFLD)是一组获得性的代谢应激相关性肝病,而晚期糖基化终末产物(AGEs)在NAFLD发病中起着重要的作用。食源性AGEs是人体内AGEs的主要贡献者,食源性AGEs可通过非受体结合的方式、受体结合的方式、影响肠道菌群发挥作用等多种机制促进NAFLD的发生与发展。AGEs特异性受体(RAGE)及RAGE下游信号通路的阻断、基因的敲除或食源性AGEs摄入限制等方法可能成为治疗此类肝病的有效手段,还需更大样本量的临床研究探求食源性AGEs影响NAFLD的确切机制。

Objective Nonalcoholic fatty liver disease(NAFLD) represents a spectrum of acquired metabolic stress-related liver diseases.The advanced glycation end products(AGEs) play an important role in the pathogenesis of NAFLD.As the main contributors to AGEs in the human body,dietary AGEs can promote the occurrence and development of NAFLD through a variety of mechanisms,including non-receptor binding,receptor binding and affecting intestinal flora.The blocking of AGE-specific cellular receptor(RAGE) and its downstream signaling pathway,gene knockout or restriction of dietary AGEs may be effective methods for the treatment of NAFLD.However,more clinical studies are needed to determine the exact mechanisms of the effect of dietary advanced glycation products on NAFLD.