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脂代谢诱导的代谢综合征发生机制

Lipid-Induced Mechanisms of Metabolic Syndrome.

机构信息

Vladivostok Branch of the Far Eastern Scientific Centre of Physiology and Pathology of Respiration, Institute of Medical Climatology and Rehabilitative Treatment, Vladivostok 690105, Russia.

Far Eastern Federal University, Vladivostok 690950, Russia.

出版信息

J Obes. 2020 Aug 26;2020:5762395. doi: 10.1155/2020/5762395. eCollection 2020.

Abstract

Metabolic syndrome (MetS) has a worldwide tendency to increase and depends on many components, which explains the complexity of diagnosis, approaches to the prevention, and treatment of this pathology. Insulin resistance (IR) is the crucial cause of the MetS pathogenesis, which develops against the background of abdominal obesity. In light of recent evidence, it has been shown that lipids, especially fatty acids (FAs), are important signaling molecules that regulate the signaling pathways of insulin and inflammatory mediators. On the one hand, the lack of n-3 polyunsaturated fatty acids (PUFAs) in the body leads to impaired molecular mechanisms of glucose transport, the formation of unresolved inflammation. On the other hand, excessive formation of free fatty acids (FFAs) underlies the development of oxidative stress and mitochondrial dysfunction in MetS. Understanding the molecular mechanisms of the participation of FAs and their metabolites in the pathogenesis of MetS will contribute to the development of new diagnostic methods and targeted therapy for this disease. The purpose of this review is to highlight recent advances in the study of the effect of fatty acids as modulators of insulin response and inflammatory process in the pathogenesis and treatment for MetS.

摘要

代谢综合征(MetS)在全球范围内呈上升趋势,且取决于许多因素,这也解释了该病理学的诊断、预防和治疗的复杂性。胰岛素抵抗(IR)是 MetS 发病机制的关键原因,它是在腹部肥胖的背景下发展起来的。根据最近的证据表明,脂质,特别是脂肪酸(FAs),是调节胰岛素和炎症介质信号通路的重要信号分子。一方面,体内缺乏 n-3 多不饱和脂肪酸(PUFAs)会导致葡萄糖转运的分子机制受损,引发未解决的炎症。另一方面,MetS 中游离脂肪酸(FFAs)的过度形成是氧化应激和线粒体功能障碍发展的基础。了解 FAs 及其代谢物参与 MetS 发病机制的分子机制将有助于开发针对这种疾病的新的诊断方法和靶向治疗。本文的目的是强调脂肪酸作为胰岛素反应和炎症过程调节剂在 MetS 发病机制和治疗中的最新研究进展。

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