INS and Obesity: In humans, IR is typically characterized as the inability of target organs of insulin action to dispose of blood glucose adequately due to increased plasma insulin concentrations, which limits endogenous glucose production (EGP), lipolysis, and the ability to induce glycogen synthesis.[5] IR is a common feature of both obesity and type 2 diabetes, and obesity is a significant factor in the development of IR in patients with T2DM.