Over-expression of CCL2/MCP-1 in adipose tissue increases macrophage recruitment and worsens the metabolic phenotype [71,72], whereas a deficiency of CCL2/MCP-1 or its receptor CCR2 reduces pro-inflammatory macrophages accumulation in adipose tissue and provides protection from insulin resistance as well as hepatic steatosis [45,71,73]. This evidence concerns the gene CCL2 and fatty liver disease.