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补体3血清水平作为肥胖中胰岛素抵抗的促炎生物标志物。

Complement 3 serum levels as a pro-inflammatory biomarker for insulin resistance in obesity.

作者信息

Al Haj Ahmad Reem M, Al-Domi Hayder A

机构信息

Department of Nutrition and Food Technology, Faculty of Agriculture, The University of Jordan, Queen Rania Street, Amman 11942, Jordan.

出版信息

Diabetes Metab Syndr. 2017 Nov;11 Suppl 1:S229-S232. doi: 10.1016/j.dsx.2016.12.036. Epub 2016 Dec 19.

DOI:10.1016/j.dsx.2016.12.036
PMID:28017633
Abstract

INTRODUCTION

Obesity is frequently characterized by chronic inflammation and insulin resistance (IR). Obesity-associated inflammation is responsible for the complement system activation of which the third component (C3) plays the central role.

OBJECTIVE

to discuss several aspects of the central component of the complement system in relation to obesity and obesity-associated IR.

METHODS

A critical review of the relevant published English articles from 2003- 2014 was carried out using several search engines including PubMed, Google Scholar, and ScienceDirect. Keywords were used, including complement system, C3, obesity-induced inflammation, IR, ASP, and adipose tissue.

CONCLUSION

The defect in the adipose tissue secretory function during obesity may result in different metabolic disorders including IR. The C3 role during obesity-associated inflammation in IR is emerging. More longitudinal studies are warranted to evaluate the role of C3 among other pro-inflammatory biomarkers for IR.

摘要

引言

肥胖常伴有慢性炎症和胰岛素抵抗(IR)。肥胖相关炎症是补体系统激活的原因,其中第三成分(C3)起着核心作用。

目的

探讨补体系统核心成分与肥胖及肥胖相关胰岛素抵抗的几个方面。

方法

使用包括PubMed、谷歌学术和ScienceDirect在内的多个搜索引擎,对2003年至2014年发表的相关英文文章进行批判性综述。使用的关键词包括补体系统、C3、肥胖诱导的炎症、IR、ASP和脂肪组织。

结论

肥胖期间脂肪组织分泌功能的缺陷可能导致包括IR在内的不同代谢紊乱。C3在肥胖相关炎症导致IR过程中的作用正在显现。需要更多的纵向研究来评估C3在其他促炎生物标志物对IR影响中的作用。

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