This improvement is likely due to several mechanisms, including reduced inflammation. Inflammation may activate NF-Kβ signaling pathways via up-regulation of TNF-α and IL-6, which stimulate hepatic CRP production [28]. TNF-α may then contribute to insulin resistance by increasing oxidation of free fatty acid (FFA), stimulating additional cytokines (i.e., IL-6), inhibiting the expression of GLUT-4 transporters, harming endothelial function, and/or impairing glucose-stimulated release of insulin by β-cells [28]. This evidence concerns the gene CRP and Insulin resistance.