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Figure 2: Low-grade chronic inflammation and oxidative stress in adipose tissue during obesity. The excessive accumulation of adipose tissue during obesity is characterized by the recruitment of immune cells. Activated T cells and chemokines induce monocyte migration into adipose tissues where they differentiate into proinflammatory M1 macrophages. The interaction between activated T cells, macrophages, and dysfunctional adipocytes results in a dysregulated adipokine and exosome-like vesicle production causing insulin resistance (IR). Adipose tissue hypoxia during obesity is associated with ROS and ox-LDL production, and foam cell formation. In addition, hypoxia and increased oxidative stress induce apoptosis of adipocytes contributing to insulin resistance.