Our official English website, www.x-mol.net, welcomes your
feedback! (Note: you will need to create a separate account there.)
An update on the potential role of advanced glycation end products in glycolipid metabolism.
Life Sciences ( IF 5.2 ) Pub Date : 2020-01-22 , DOI: 10.1016/j.lfs.2020.117344 Xiaolei Wang 1 , Junjun Liu 1 , Ying Yang 1 , Xiandang Zhang 1
Life Sciences ( IF 5.2 ) Pub Date : 2020-01-22 , DOI: 10.1016/j.lfs.2020.117344 Xiaolei Wang 1 , Junjun Liu 1 , Ying Yang 1 , Xiandang Zhang 1
Affiliation
|
Advanced glycation end products (AGEs) play a crucial role in many major diseases, such as diabetes and atherosclerosis. AGE accumulation in the body is generally considered a consequence of hyperglycaemia. However, recent studies have shown that AGEs may also be an important cause of the initial pathogenesis of diabetes and atherosclerosis. The objective of the present review is to provide an update on the AGE-induced mechanisms involved in the pathophysiology of glucose and lipid metabolism, even though the unique mechanisms involved in these diseases are not well understood. AGE precursors (methylglyoxal) and AGE receptors have been demonstrated in animal models to mediate insulin resistance and lipid metabolism disorders. Although we have not yet achieved a complete understanding of the role of AGEs, emerging therapeutic interventions targeting AGE reduction and AGE-RAGE signalling have yielded some beneficial clinical outcomes. Additional studies are needed to evaluate the utility and mechanism of circulating and tissue AGEs to support the identification of efficient and specific interventions.
中文翻译：
有关高级糖基化终产物在糖脂代谢中潜在作用的更新。
晚期糖基化终末产物（AGEs）在许多主要疾病（例如糖尿病和动脉粥样硬化）中起着至关重要的作用。体内AGE的积累通常被认为是高血糖症的结果。但是，最近的研究表明，AGEs可能也是糖尿病和动脉粥样硬化初始发病机制的重要原因。本综述的目的是提供有关AGE诱导的葡萄糖和脂质代谢的病理生理学机制的更新，即使尚未很好地了解这些疾病涉及的独特机制。在动物模型中已证明AGE前体（甲基乙二醛）和AGE受体可介导胰岛素抵抗和脂质代谢紊乱。尽管我们尚未完全了解AGE的作用，针对AGE减少和AGE-RAGE信号转导的新兴治疗性干预已产生了一些有益的临床结果。需要进行其他研究来评估循环和组织AGEs的效用和机制，以支持对有效和特异性干预措施的鉴定。
更新日期：2020-01-22
中文翻译：
有关高级糖基化终产物在糖脂代谢中潜在作用的更新。
晚期糖基化终末产物（AGEs）在许多主要疾病（例如糖尿病和动脉粥样硬化）中起着至关重要的作用。体内AGE的积累通常被认为是高血糖症的结果。但是，最近的研究表明，AGEs可能也是糖尿病和动脉粥样硬化初始发病机制的重要原因。本综述的目的是提供有关AGE诱导的葡萄糖和脂质代谢的病理生理学机制的更新，即使尚未很好地了解这些疾病涉及的独特机制。在动物模型中已证明AGE前体（甲基乙二醛）和AGE受体可介导胰岛素抵抗和脂质代谢紊乱。尽管我们尚未完全了解AGE的作用，针对AGE减少和AGE-RAGE信号转导的新兴治疗性干预已产生了一些有益的临床结果。需要进行其他研究来评估循环和组织AGEs的效用和机制，以支持对有效和特异性干预措施的鉴定。
京公网安备 11010802027423号