Ccrl2 deficiency deteriorates obesity and insulin resistance through increasing adipose tissue macrophages infiltration

Genes and Diseases

Jun Li¹  Cheng-Long Huang¹  Min Xu¹  Wen-Hua Xie¹  Lin-Fen Tao¹  Yu-Meng Wang¹  Hong-Xiang Zeng¹  Wan-Qing Li¹  Xi Li² 

[1] Biology Science Institutes, Chongqing Medical University, Chongqing 400016, PR China;Corresponding author. Biology Science Institutes, Chongqing Medical University, 1 Yi Xue Yuan Road, Chongqing, 400032, PR China.;

关键词: Ccrl2;    Inflammation;    Insulin resistance;    Macrophages;    Obesity;   

DOI  :  

来源: DOAJ

【 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.

【 授权许可】

Unknown