Editorial Insulin Resistance, Type 1 and Type 2 Diabetes, and Related Complications 2015

Copyright © 2015 Joseph Fomusi Ndisang et al.This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The dramatic increase in obesity and diabetes worldwide poses a huge socioeconomic burden to healthcare systems. In type 1 diabetes, autoimmune-mediated destruction of pan-creatic beta-cell results in insulin deficiency [1]. Obesity is one of the major causes of type 2 diabetes [1–3]. In type 2 diabetes, a combination of peripheral insulin resistance and aberrant production of insulin are amongst the paradox commonly encountered in the pathogenesis of the disease [1– 3]. However, both forms of diabetes are characterized by ele-vated inflammation/oxidative stress, glucotoxicity, lipotox-icity, endoplasmic reticulum-induced stress with increased apoptosis and necrosis that ultimately leads to destruc