肥胖症代谢紊乱的一个新方面:羰基压力

A. Lesnaya, M. Darenskaya, N. Semenova, L. Kolesnikova
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引用次数: 0

摘要

文献综述探讨了现代社会的肥胖问题。研究表明,肥胖会加重伴随疾病,增加患代谢紊乱和相关病症的概率,增加并发症和死亡风险。研究详细探讨了脂肪组织的分泌功能及其参与调节生物过程的情况。揭示了羰基应激的概念及其组成部分,描述了羰基化合物在体内的作用,展示了导致羰基反应产物形成的代谢途径,指出了自由基在这些代谢途径中的参与。讨论了与肥胖症羰基压力发展相关的发病机制;肥胖症羰基病理学发展的最大贡献来自两类过程:脂质过氧化反应导致脂质过氧化羰基产物的形成,以及高血糖激活的过程(糖酵解、多元醇和六оz胺途径)导致乙二醛、甲基乙二醛和葡萄糖的活性羰基形式的形成。关于高级糖化终产物(AGEs)和高级氧化蛋白产物(AOРР)对肥胖症羰基病理学发展的贡献,目前仍存在争议。据推测,AGEs 和 AOРР 的水平取决于肥胖的严重程度和代谢综合征的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A new aspect of metabolic disorders in obesity: carbonyl stress
The literature review examines the problem of obesity in modern society. It has been shown that obesity aggravates concomitant diseases, increases the probability of developing metabolic disorders and related pathologies, increases the risk of complications and mortality. The secretory function of adipose tissue, its participation in the regulation of biological processes is considered in detail. The concept of carbonyl stress and its components is revealed, the role of carbonyl compounds in the body is described, the metabolic pathways leading to the formation of carbonyl reaction products are shown, the participation of free radicals in these metabolic pathways is noted. The mechanisms of pathogenesis associated with the development of carbonyl stress in obesity are discussed; the greatest contribution to the development of car bonyl pathology in obesity is made by two types of processes: lipid peroxidation reactions resulting in the formation of carbonyl products of lipoperoxidation and the processes activated by hyperglycemia (glycolysis, polyol and hexоzamine pathways) leading to the formation of glyoxal, methylglyoxal, and active carbonyl forms of glucose. The question of the contribution of advanced glycation end products (AGEs) and advanced oxidation protein products (AOРР) to the development of carbonyl pathology in obesity remains controversial. It is assumed that AGEs and AOРР levels depend on the severity of obesity and the development of metabolic syndrome.
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