Type 2 diabetes (T2D) is a complex multifactorial disorder for which the etiology is still a cause for debate. However it is generally accepted that dysregulated glucose sensing and (or) insulin secretion leading to insufficient compensation for peripheral insulin resistance is a major feature of the pathogenesis of TD2 (Patarrao et al. 2012). The prevalence of this chronic disease is a global public health concern, and insufficient health care guidelines have been developed to address its prevention based on education, lifestyle intervention, and therapeutics. On the other hand, there is already comprehensive knowledge about insulin signaling and insulin receptor substrates (irs), specifically irsl and irs2, which mediate the pleiotropic effects of insulin. Irsl acts mainly in skeletal muscle insulin signaling and growth, whereas irs2 is widely expressed and has a broader role in insulin signaling. The paper by Oliveira et al. in this issue of CJPP reviews the role of irs2 in several perspectives, highlighting the involvement of irs2 in protecting against beta-cell failure; an important feature of all types of diabetes. Moreover, irs2 is also relevant for the maintenance of glucose metabolism in T2D. White et al. contributed to establishing this theory when they found that irs2-deficient mice develop diabetes (Withers et al. 1999; White 2006).
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