insulin because of insulin resistance would thus result in the activation of these proinflammatory transcription factors and an increase in the expression of the corresponding genes. Insulin has been shown to suppress NF-κB binding activity, reactive oxygen species (ROS) generation, and p47phox expression and to increase IκB expression in mononuclear cells (MNCs) as well as to suppress plasma concentrations of intercellular adhesion molecule-1 and monocyte chemotactic protein-1. 16 In addition, insulin suppresses AP-1 and Egr-1, 2 proinflammatory transcription factors and their respective genes, matrix metalloproteinase-9, tissue factor (TF), and PAI-1. 17–19 Thus, insulin has a comprehensive antiinflammatory effect and in addition has an antioxidant effect, as reflected in the suppression of ROS generation and p47phox expression (Figure 1). 16, 20