SLC2A4 and Insulin resistance: Specifically regarding IL-6 and TNF-α [45], both are responsible for stimulation of the IκB kinase-β (IKK-β)/nuclear factor-κB (NF-κB) and the c-Jun aminoterminal kinase (JNK) through specific receptors, elevating inflammation, impairing insulin signaling [46], besides the downregulation of glucose transporters (GLUT-4) causing insulin resistance in the long run [47].