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膳食晚期糖基化终末产物(AGEs):预防与衰老相关的慢性疾病的一个可改变的风险因素?

Dietary advanced glycation end products (AGEs): A modifiable risk factor in the prevention of chronic diseases associated with aging?

作者信息

Ávila Felipe, Cruz Nadia, González Ma Angélica, Fuentes Eduardo, Wehinger Sergio, Lutz Mariane

机构信息

Department of Nutrition and Food Science, School of Nutrition and Dietetics, Health Science Faculty, Campus Lircay, University of Talca, Talca, 3480094, Chile; Interuniversity Center for Healthy Aging (CIES), Universidad de Talca, Talca, 3480094, Chile; VITALIS, Centro de Longevidad, Universidad de Talca, Talca, 3480094, Chile.

Department of Nutrition and Food Science, School of Nutrition and Dietetics, Health Science Faculty, Campus Lircay, University of Talca, Talca, 3480094, Chile.

出版信息

Biochimie. 2025 Aug;235:80-92. doi: 10.1016/j.biochi.2025.06.001. Epub 2025 Jun 3.

DOI:10.1016/j.biochi.2025.06.001
PMID:40473013
Abstract

Advanced glycation end products (AGEs) are a heterogeneous group of compounds formed during the advanced stages of the Maillard reaction through non-enzymatic reactions, occurring mainly between reducing sugars or their oxidation metabolites and amino groups in proteins, lipids, and nucleic acids. These compounds can be endogenously formed, particularly under hyperglycemic conditions. In addition, AGEs are also produced exogenously during the thermal processing of foods, contributing to the dietary intake of these compounds. The accumulation of AGEs in body tissues has been associated with aging and the pathogenesis of various non-communicable diseases. Dietary intake of AGEs contributes significantly to their systemic burden. Consequently, reducing the intake of dietary AGEs has been proposed as a modifiable risk factor for the prevention of chronic, age-related diseases. This review examines and discusses current evidence on the molecular mechanisms by which dietary and endogenous AGEs contribute to cellular senescence and the progression of prevalent age-associated pathologies, including diabetes, cardiovascular diseases, musculoskeletal disorders, and neurodegeneration.

摘要

晚期糖基化终末产物(AGEs)是一组异质性化合物,在美拉德反应的晚期通过非酶促反应形成,主要发生在还原糖或其氧化代谢产物与蛋白质、脂质和核酸中的氨基之间。这些化合物可以内源性形成,尤其是在高血糖条件下。此外,AGEs也在食品热加工过程中外源性产生,导致这些化合物的膳食摄入。AGEs在人体组织中的积累与衰老和各种非传染性疾病的发病机制有关。膳食中AGEs的摄入对其全身负担有显著影响。因此,减少膳食中AGEs的摄入已被提议作为预防慢性、与年龄相关疾病的一个可改变的风险因素。本综述研究并讨论了当前关于膳食和内源性AGEs导致细胞衰老以及常见的与年龄相关病理进展(包括糖尿病、心血管疾病、肌肉骨骼疾病和神经退行性变)的分子机制的证据。

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