@article{Xu2022, 
author = {Min Xu and Yu-Meng Wang and Wan-Qing Li and Cheng-Long Huang and Jun Li and Wen-Hua Xie and Hong-Xiang Zeng and Lin-Fen Tao and Xi Li},
title = {Ccrl2 deficiency deteriorates obesity and insulin resistance through increasing adipose tissue macrophages infiltration},
year = {2022},
journal = {Genes & Diseases},
volume = {9},
number = {2},
pages = {429-442},
keywords = {Ccrl2, Inflammation, Insulin resistance, Macrophages, Obesity},
url = {https://www.sciopen.com/article/10.1016/j.gendis.2020.08.009},
doi = {10.1016/j.gendis.2020.08.009},
abstract = {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.}
}