Ccrl2 deficiency deteriorates obesity and insulin resistance through increasing adipose tissue macrophages infiltration
作者机构：Biology Science InstitutesChongqing Medical UniversityChongqing 400016PR China
出 版 物：《Genes & Diseases》 (基因与疾病（英文）)
年 卷 期：2022年第9卷第2期
页 面：429-442页
核心收录：
学科分类：0710[理学-生物学] 0831[工学-生物医学工程（可授工学、理学、医学学位）] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 0703[理学-化学] 10[医学]
基 金：This work was supported by National Key R&D Program of China(No.2018YFA0800401 to X.Li) National Natural Science Foundation of China(No.81770861 and 31571401 to X.Li) Chongqing Science and Technology Foundation(No.cstc2018jcyjAX0232) Science and Technology Research Program of Chongqing Municipal Education Commission(No.KJZD-K201800402).
主 题：Ccrl2 Inflammation Insulin resistance Macrophages Obesity
摘 要：Obesity-induced inflammation,characterized by augmented infiltration and altered balance of macrophages,is a critical component of systemic insulin resistance.Chemokine-chemokine receptor system plays a vital role in the macrophages accumulation.CC-Chemokine Receptor-like 2(Ccrl2)is one of the receptors of Chemerin,which is a member of atypical chemokine receptors(ACKR)family,reported taking part in host immune responses and inflammation-related conditions.In our study,we found ccrl2 expression significantly elevated in visceral adipose tissue(VAT)of high fat diet(HFD)induced obese mice and ob/ob mice.Systemic deletion of Ccrl2 gene aggravated HFD induced obesity and insulin resistance and ccrl2−/−mice showed aggravated VAT inflammation and increased M1/M2 macrophages ratio,which is due to the increase of macrophages chemotaxis in Ccrl2 deficiency mice.Cumulatively,these results indicate that Ccrl2 has a critical function in obesity and obesity-induced insulin resistance via mediating macrophages chemotaxis.
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