Fig. 6

Chemokines-induced IR. M2 macrophages in lean state, maintain the insulin sensitivity in adipose tissues whereas, due to overnutrition, adipose tissues initiates the secretion of MCP-1 which leads to the recruitment of circulating monocytes in adipocytes. CCR2 macrophages are accumulated in obese adipocytes and presumably maintain the inflammation by recruiting M1 macrophages in obese adipocytes. While on the other side, CCR5-adipose tissue macrophages (ATM) also infiltrate from the obese adipocytes and promote the inflammatory responses by involving ATM recruitment and producing various pro-inflammatory mediators notably TNF-α, IL-6, and IL-1β in conjunction with other infiltrated immune cells and adipokines. After production, these pro-inflammatory mediators induce IR in adipocytes and peripheral tissues through activation of several transcriptional pathways such as JNK and NF-κB. Adapted from Xu et al. 2015