Figure 1: Schematic illustration of some of the key pathophysiological aspects involved in the development of T2DM, focusing on the involvement of oxidative stress and inflammation and underlying cellular/molecular mechanisms. AGEs, advanced glycation end-products; COXs, cyclooxygenases; CRP, C-reactive protein; GLUT, glucose transporter; GSH, endogenous antioxidant glutathione; iCAM, intracellular adhesion molecule-1; IL-1β, interleukin 1β; IL-6, interleukin 6; JNK, Jun N-terminal kinase; p38-MAPK, mitogen-activated protein kinase; NADPH, nicotinamide adenine dinucleotide phosphate; NF-KB, factor nuclear kappa B; NO, nitric oxide; PKC, protein kinase C; RAGE, receptor of advanced glycation end-products; TNF-α, tumor necrosis factor alpha; vCAM, vascular cell adhesion molecule.