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The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction.
Molecular Nutrition & Food Research ( IF 4.5 ) Pub Date : 2020-04-04 , DOI: 10.1002/mnfr.201900934
Domenico Sergi 1, 2 , Hakim Boulestin 3 , Fiona M Campbell 3 , Lynda M Williams 3
Affiliation  

Advanced glycation end products (AGEs) are a heterogeneous group of molecules produced, non‐enzymatically, from the interaction between reducing sugars and the free amino groups of proteins, nucleic acids, and lipids. AGEs are formed as a normal consequence of metabolism but can also be absorbed from the diet. They have been widely implicated in the complications of diabetes affecting cardiovascular health, the nervous system, eyes, and kidneys. Increased levels of AGEs are also detrimental to metabolic health and may contribute to the metabolic abnormalities induced by the Western diet, which is high in processed foods and represents a significant source of AGEs. While increased AGE levels are a consequence of diabetic hyperglycaemia, AGEs themselves activate signaling pathways, which compromise insulin signaling and pancreatic β‐cell function, thus, contributing to the development of type 2 diabetes mellitus (T2DM). Furthermore, AGEs may also contribute to the obesogenic effects of the Western diet by promoting hypothalamic inflammation and disrupting the central control of energy balance. Here, the role of dietary AGEs in metabolic dysfunction is reviewed with a focus on the mechanisms underpinning their detrimental role in insulin resistance, pancreatic β‐cell dysfunction, hypothalamic control of energy balance, and the pathogenesis of T2DM and obesity.

中文翻译:

膳食高级糖化终产物在代谢功能障碍中的作用。

晚期糖基化终产物 (AGEs) 是由还原糖与蛋白质、核酸和脂质的游离氨基之间的相互作用以非酶促方式产生的一组异质分子。AGEs 是新陈代谢的正常结果,但也可以从饮食中吸收。它们广泛地与影响心血管健康、神经系统、眼睛和肾脏的糖尿病并发症有关。AGEs 水平升高也对代谢健康有害,并可能导致西方饮食引起的代谢异常,西方饮食中含有大量加工食品,是 AGEs 的重要来源。虽然 AGE 水平升高是糖尿病高血糖的结果,但 AGE 本身会激活信号通路,从而损害胰岛素信号和胰腺 β 细胞功能,因此,促进了 2 型糖尿病 (T2DM) 的发展。此外,AGEs 还可能通过促进下丘脑炎症和破坏能量平衡的中枢控制而导致西方饮食的致胖效应。本文综述了膳食 AGEs 在代谢功能障碍中的作用,重点关注其在胰岛素抵抗、胰腺 β 细胞功能障碍、下丘脑控制能量平衡以及 T2DM 和肥胖发病机制中的有害作用的机制。
更新日期:2020-04-04
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