We found a) impairment of systemic insulin sensitivity by PM2.5 in WT but not CCR2–/– mice; b) CCR2-dependent potentiation of VAT inflammation and impairment of AMPK and AKT signaling by PM2.5; c) CCR2-dependent enhancement of hepatic lipogenesis/steatosis and activation of p38 MAPK and reduction of insulin signaling by PM2.5; and d) worsening of fasting hyperglycemia via CCR2-independent nongluconeogenic mechanisms. The gene discussed is AKT1; the disease is steatosis.