Abstract

Type 2 diabetes (T2D) is a metabolic disorder that is accompanied by chronic inflammation. The main mechanisms and molecular signaling of the induction of inflammation in T2D are still unknown. It seems that intracellular sensors that participate in recognition of endogenous damage associated molecular patterns (DAMPs) play key roles in the induction/stimulation of chronic inflammation in T2D. The Nucleotide-binding oligomerization domain, Leucine-rich Repeat and Pyrin domain containing (NLRP) family and accompanying Inflammasomes are important intracellular receptors of inflammatory pathogens and stress signals that elevate caspase-l-mediated release of IL-1 beta and IL-18. Studies suggest that disruption of NLRP1 and NLRP3 has a major role for these inflammasomes in internal immunity and inflammation as well as metabolic disorders. Thus, it seems that these mediators may participate in the induction/stimulation of chronic inflammation in patients. This systematic review provides an up-to-date evaluation of our current understanding of the roles of inflammasomes in the pathogenesis of T2D and its complications.