Since inflammatory monocytes recruit via CCR2 in response to CCL2 (MCP-1) in adipose tissue during pathogenic expansion leading to insulin resistance, we next determined whether peripheral blood monocytes of ERV1tg mice may be skewed to patrolling (CCR2-CX3CR1high, M2-like) relative to inflammatory (CCR2+CX3CR1int, M1-like) phenotype under dietary fat overload8,9. This evidence concerns the gene CCR2 and Insulin resistance.