Published online May 26, 2017. doi: 10.4331/wjbc.v8.i2.120
Peer-review started: November 29, 2016
First decision: January 16, 2017
Revised: January 24, 2017
Accepted: February 18, 2017
Article in press: February 19, 2017
Published online: May 26, 2017
Processing time: 173 Days and 5.8 Hours
Core tip: Low-grade inflammation of adipose tissue (AT) contributes to insulin resistance and type 2 diabetes in obese patients. On the contrary, in lean individuals, the immune environment of AT is non-inflammatory. In obesity, AT is infiltrated by pro-inflammatory macrophages and T cells leading to the accumulation of interleukin-1β (IL-1β), tumor necrosis factor α, IL-17 and IL-6. On the contrary, M2 macrophages, Th2 and T-regs cells producing anti-inflammatory IL-10, IL-5 and interferon-γ, are present in AT of lean individuals. Here, we discuss the interaction between AT and infiltrating immune cells in the lean vs the obese condition, with emphasis on the contribution of pro- and anti-inflammatory cytokines to the establishment of insulin resistance.