A deficiency of MCP-1 (CCL2) or CCR2 (CCL2 receptor) in mice results in the impairment of pro-inflammatory macrophage recruitment to adipose tissue, thus impeding the induction of insulin resistance (Kanda et al., 2006; Yu et al., 2006) and suggesting an important role for pro-inflammatory macrophages in the initiation and development of diabetes. Here, CCL2 is linked to diabetes mellitus.