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

BACKGROUND: Chronic exposure to fine ambient particulate matter (PM(2.5)) 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 PM(2.5) exposure-mediated inflammation leading to insulin resistance under high fat diet situation. The present study assessed the importance of CCR2 in PM(2.5) 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 PM(2.5) or filtered air for 6 months. In C57BL/6 mice, concentrated ambient PM(2.5) 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 PM(2.5)-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 PM(2.5) exposure-induced insulin resistance in mice fed on normal diet. The present study indicates that PM(2.5) may dysregulate glucose metabolism directly without exerting proinflammatory effects. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12989-017-0187-3) contains supplementary material, which is available to authorized users.