CCL2 and Insulin resistance: Adipose tissue-specific overexpression of MCP-1 in mice indeed increased macrophage infiltration into adipose tissue and insulin resistance (17, 19), whereas disruption of MCP-1 or its receptor, CCR2, impaired high-fat diet (HFD)-induced migration of macrophages into adipose tissue, thereby reducing adipose tissue inflammation and attenuating insulin resistance (17, 18, 29, 30).