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代谢综合征是一种炎症性疾病:脂肪组织和吞噬细胞之间的共谋。

Metabolic syndrome is an inflammatory disorder: A conspiracy between adipose tissue and phagocytes.

机构信息

California Northstate University, College of Medicine, Elk Grove, CA 95757, USA.

California Northstate University, College of Medicine, Elk Grove, CA 95757, USA; VA Medical Center, Mather, CA 95757, USA.

出版信息

Clin Chim Acta. 2019 Sep;496:35-44. doi: 10.1016/j.cca.2019.06.019. Epub 2019 Jun 20.

DOI:10.1016/j.cca.2019.06.019
PMID:31229566
Abstract

Metabolic syndrome (MetS) describes a cluster of cardio-metabolic factors that predispose to type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease (ASCVD). While 35% of Americans suffer from this disorder, the specific pathways related to this disease are largely underexplored. The prevailing consensus is that inflammatory pathways contribute to the pathogenesis of this disease, and therefore new research has uncovered how inflammation plays a critical role in the development and progression of MetS. The purpose of this review is to understand the role of major inflammatory mechanisms and their role in MetS. Our review identifies that adipose tissue (AT) contributes to the inflammatory pathways through the release of pro-inflammatory adipokines such as leptin and chemerin and dysregulation of anti-inflammatory adiponectin. Chemokines and cytokines deriving from monocytes are also altered and promote inflammation and insulin resistance. Circulating inflammatory biomarkers including C-reactive protein (CRP), fibrinogen, Serum amyloid A (SAA), cytokines, and chemokines have also been linked to the pathogenesis of MetS. Researchers have identified the significance of CRP levels in predicting future sequelae of MetS such as ASCVD. Mast cells in subcutaneous adipose tissue (SAT) promote both inflammation and fibrosis. Thus, both AT and phagocyte activity define MetS as an inflammatory disorder.

摘要

代谢综合征(MetS)描述了一组心血管代谢因素,这些因素易导致 2 型糖尿病(T2DM)和动脉粥样硬化性心血管疾病(ASCVD)。虽然 35%的美国人患有这种疾病,但与这种疾病相关的具体途径在很大程度上尚未得到探索。目前的共识是,炎症途径有助于这种疾病的发病机制,因此新的研究已经揭示了炎症如何在代谢综合征的发展和进展中发挥关键作用。本综述的目的是了解主要炎症机制及其在代谢综合征中的作用。我们的综述确定脂肪组织(AT)通过释放促炎脂肪因子(如瘦素和趋化素)和抗炎脂联素的失调来促进炎症途径。源自单核细胞的趋化因子和细胞因子也发生改变,并促进炎症和胰岛素抵抗。循环炎症生物标志物,包括 C 反应蛋白(CRP)、纤维蛋白原、血清淀粉样蛋白 A(SAA)、细胞因子和趋化因子,也与代谢综合征的发病机制有关。研究人员已经确定 CRP 水平在预测代谢综合征如 ASCVD 的未来后果方面的重要性。皮下脂肪组织(SAT)中的肥大细胞促进炎症和纤维化。因此,脂肪组织和吞噬细胞活性都将代谢综合征定义为一种炎症性疾病。

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