Aragno Manuela, Mastrocola Raffaella
Department of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125 Turin, Italy.
Nutrients. 2017 Apr 14;9(4):385. doi: 10.3390/nu9040385.
The rapid increase in metabolic diseases, which occurred in the last three decades in both industrialized and developing countries, has been related to the rise in sugar-added foods and sweetened beverages consumption. An emerging topic in the pathogenesis of metabolic diseases related to modern nutrition is the role of Advanced Glycation Endproducts (AGEs). AGEs can be ingested with high temperature processed foods, but also endogenously formed as a consequence of a high dietary sugar intake. Animal models of high sugar consumption, in particular fructose, have reported AGE accumulation in different tissues in association with peripheral insulin resistance and lipid metabolism alterations. The in vitro observation that fructose is one of the most rapid and effective glycating agents when compared to other sugars has prompted the investigation of the in vivo fructose-induced glycation. In particular, the widespread employment of fructose as sweetener has been ascribed by many experimental and observational studies for the enhancement of lipogenesis and intracellular lipid deposition. Indeed, diet-derived AGEs have been demonstrated to interfere with many cell functions such as lipid synthesis, inflammation, antioxidant defences, and mitochondrial metabolism. Moreover, emerging evidence also in humans suggest that this impact of dietary AGEs on different signalling pathways can contribute to the onset of organ damage in liver, skeletal and cardiac muscle, and the brain, affecting not only metabolic control, but global health. Indeed, the most recent reports on the effects of high sugar consumption and diet-derived AGEs on human health reviewed here suggest the need to limit the dietary sources of AGEs, including added sugars, to prevent the development of metabolic diseases and related comorbidities.
在过去三十年中，工业化国家和发展中国家的代谢性疾病都迅速增加，这与添加糖食品和含糖饮料的消费增加有关。与现代营养相关的代谢性疾病发病机制中的一个新兴话题是晚期糖基化终产物（AGEs）的作用。AGEs可以通过高温加工食品摄入，也可因高糖饮食而内源性形成。高糖饮食的动物模型，特别是果糖摄入模型，已报道不同组织中AGEs的积累与外周胰岛素抵抗和脂质代谢改变有关。与其他糖类相比，果糖是体外观察到的最快速有效的糖化剂之一，这促使人们对体内果糖诱导的糖化进行研究。特别是，许多实验和观察性研究将果糖作为甜味剂的广泛使用归因于脂肪生成的增强和细胞内脂质沉积。事实上，饮食来源的AGEs已被证明会干扰许多细胞功能，如脂质合成、炎症、抗氧化防御和线粒体代谢。此外，人类的新证据也表明，饮食AGEs对不同信号通路的这种影响可能导致肝脏、骨骼肌和心肌以及大脑器官损伤的发生，不仅影响代谢控制，还影响整体健康。的确，此处综述的关于高糖饮食和饮食来源的AGEs对人类健康影响的最新报告表明，需要限制包括添加糖在内AGEs的饮食来源以预防代谢性疾病及相关合并症的发生。
