Metabolic impairments associated with obesity may contribute to the release of inflammatory mediators (IL-18, IL-1β) due to the stimulation of the NLR (nucleotide-binding oligomerization domain (NOD)-like receptors) family pyrin domain-containing 3 (NLRP3) which forms a cytoplasmic complex known as the NLRP3 inflammasome, with direct modulating role on the innate immune system. This pathway is involved in obesity as well as associated inflammation, and among the endogenous danger signals activating it we can find glucose and ROS. Also, literature data states that IL-18 as well as IL-1β are produced as an effect of TLR (Toll-like receptors)-mediated NF-κB activation, thus pointing out to the interaction of different signalling pathways (Fettelschoss et al., 2011; Tschopp and Schroder, 2010; Zhou et al., 2010).