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.