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慢性炎症状态的机制作为连接肥胖脂肪组织和代谢综合征的介质。

Mechanisms of chronic state of inflammation as mediators that link obese adipose tissue and metabolic syndrome.

机构信息

Immunology and Haematology Laboratory, Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Interdisciplinary Excellence Research Program on Healthy Aging, Universidad de Talca, Talca, Chile.

出版信息

Mediators Inflamm. 2013;2013:136584. doi: 10.1155/2013/136584. Epub 2013 Jun 13.

DOI:10.1155/2013/136584
PMID:23843680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3697419/
Abstract

The metabolic syndrome is a cluster of cardiometabolic alterations that include the presence of arterial hypertension, insulin resistance, dyslipidemia, and abdominal obesity. Obesity is associated with a chronic inflammatory response, characterized by abnormal adipokine production, and the activation of proinflammatory signalling pathways resulting in the induction of several biological markers of inflammation. Macrophage and lymphocyte infiltration in adipose tissue may contribute to the pathogenesis of obesity-mediated metabolic disorders. Adiponectin can either act directly on macrophages to shift polarization and/or prime human monocytes into alternative M2-macrophages with anti-inflammatory properties. Meanwhile, the chronic inflammation in adipose tissue is regulated by a series of transcription factors, mainly PPARs and C/EBPs, that in conjunction regulate the expression of hundreds of proteins that participate in the metabolism and storage of lipids and, as such, the secretion by adipocytes. Therefore, the management of the metabolic syndrome requires the development of new therapeutic strategies aimed to alter the main genetic pathways involved in the regulation of adipose tissue metabolism.

摘要

代谢综合征是一组与心血管代谢相关的改变,包括动脉高血压、胰岛素抵抗、血脂异常和腹部肥胖的存在。肥胖与慢性炎症反应有关,其特征是异常脂联素的产生,以及促炎信号通路的激活,导致多种炎症生物标志物的诱导。脂肪组织中巨噬细胞和淋巴细胞的浸润可能有助于肥胖介导的代谢紊乱的发病机制。脂联素可以直接作用于巨噬细胞,改变其极化状态,或将人单核细胞诱导为具有抗炎特性的替代性 M2 巨噬细胞。同时,脂肪组织中的慢性炎症受一系列转录因子(主要是 PPARs 和 C/EBPs)的调节,这些转录因子共同调节数百种参与脂质代谢和储存的蛋白质的表达,从而调节脂肪细胞的分泌。因此,代谢综合征的管理需要开发新的治疗策略,旨在改变调节脂肪组织代谢的主要遗传途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40c8/3697419/59e02999dff8/MI2013-136584.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40c8/3697419/43d36a0881ab/MI2013-136584.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40c8/3697419/59e02999dff8/MI2013-136584.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40c8/3697419/43d36a0881ab/MI2013-136584.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40c8/3697419/59e02999dff8/MI2013-136584.002.jpg

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