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饮食源性晚期糖基化终产物及其与糖尿病炎症的关系——综述。

Advanced glycation end products of dietary origin and their association with inflammation in diabetes - A minireview.

机构信息

Catedra de Inmunologia, Escuela de Bioanalisis, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela.

Hospital General Andino, Riobamba, Ecuador.

出版信息

Endocr Regul. 2024 Apr 2;58(1):57-67. doi: 10.2478/enr-2024-0007. Print 2024 Jan 1.

Abstract

Advanced glycation end products (AGEs) are a diverse group of compounds that are formed as a result of the non-enzymatic reaction between a reducing sugar such as glucose and the free NH2 groups of an amino acid in a protein or other biomolecule. The chemical reaction, by which these products are generated, is known as the Maillard reaction and occurs as a part of the body's normal metabolism. Such a reaction is enhanced during diabetes due to hyperglycemia, but it can also occur during the preparation, processing, and preservation of certain foods. Therefore, AGEs can also be obtained from the diet (d-AGE) and contribute to an increase of the total serum pool of these compounds. They have been implicated in a wide variety of pathological processes, mainly because of their ability to induce inflammatory responses and oxidative stress increase. They are extensively accumulated as a part of the normal aging, especially in tissues rich in long half-life proteins, which can compromise the physiology of these tissues. d-AGEs are abundant in diets rich in processed fats and sugars. This review is addressed to the current knowledge on these products and their impact on the immunomodulation of various mechanisms that may contribute to exacerbation of the diabetes pathophysiology.

摘要

糖基化终产物(AGEs)是一组多样化的化合物,是由还原糖(如葡萄糖)与蛋白质或其他生物分子中氨基酸的游离 NH2 基团之间的非酶反应形成的。这种产物生成的化学反应称为美拉德反应,是身体正常代谢的一部分。由于高血糖,这种反应在糖尿病中会增强,但它也可能在某些食物的制备、加工和保存过程中发生。因此,AGEs 也可以从饮食中获得(d-AGE),并导致这些化合物的总血清池增加。它们与广泛的病理过程有关,主要是因为它们能够诱导炎症反应和增加氧化应激。它们作为正常衰老的一部分广泛积累,特别是在富含半衰期长的蛋白质的组织中,这会损害这些组织的生理学。富含加工脂肪和糖的饮食中含有大量的 d-AGE。本文综述了这些产物的最新知识及其对各种机制免疫调节的影响,这些机制可能导致糖尿病病理生理学的恶化。

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