Recently, Wen et al. [32] demonstrated in macrophages that palmitate, a saturated fatty acid, could activate NLRP3 whereas the unsaturated oleate was not responsive. Interestingly, NLRP3 activation was ROS-dependent and secreted IL-1β impaired insulin signaling and promoted insulin resistance in mice. Vandanmagsar et al. [33] revealed that obesity was associated with the activation of NLRP3 in adipose tissue. These workers observed that the weight loss of obese humans, induced by caloric restriction and exercise, was associated with (i) a reduction of NLRP3 expression in adipose tissue, (ii) a decrease in the level of inflammation and (iii) an increase in insulin sensitivity. Supporting these results, Stienstra et al. [34] observed that transgenic mice which lack Nlrp3, Asc and caspase-1genes were resistant to the obesity induced by high-fat diet and protected from insulin resistance. It seems that NLRP3 could be a sensor for metabolic stress recognizing ROS production [35]. Tschopp and Schroder [36] speculated that different danger signal pathways converge and activate NLRP3 inflammasomes via ROS production.
