Particulate Air pollution mediated effects on insulin resistance in mice are independent of CCR2

Background: chronic exposure to fine ambient particulate matter (pm2.5) induces insulin resistance. cc-chemokine receptor 2 (ccr2) appears to be essential in diet-induced insulin resistance implicating an important role for systemic cellular inflammation in the process. we have previously suggested that ccr2 is important in pm2.5 exposure-mediated inflammation leading to insulin resistance under high fat diet situation. the present study assessed the importance of ccr2 in pm2.5 exposure-induced insulin resistance in the context of normal diet. methods and results: c57bl/6 and ccr2-/- mice were subjected to exposure to concentrated ambient pm2.5 or filtered air for 6 months. in c57bl/6 mice,concentrated ambient pm2.5 exposure induced whole-body insulin resistance,macrophage infiltration into the adipose tissue,and upregulation of phosphoenolpyruvate carboxykinase (pepck) in the liver. while ccr2 deficiency reduced adipose macrophage content in the pm2.5-exposed animals,it did not improve systemic insulin resistance. this lack of improvement in insulin resistance was paralleled by increased hepatic expression of genes in pepck and inflammation. conclusion: ccr2 deletion failed to attenuate pm2.5 exposure-induced insulin resistance in mice fed on normal diet. the present study indicates that pm2.5 may dysregulate glucose metabolism directly without exerting proinflammatory effects. © 2017 the author(s).