Adiponectin inhibits NLRP3 inflammasome by modulating the AMPK-ROS pathway.

Chronic inflammation is a key contributor to obesity-related insulin resistance and type 2 diabetes (T2D). NLRP3 inflammasome activation plays an important role in impairing insulin signaling and insulin sensitivity. Adiponectin is an adipocyte-derived cytokine that has been shown to promote insulin sensitivity and exert anti-inflammatory properties, yet the detailed mechanism is still unclear. In this study, we aimed to investigate the anti-inflammatory effect of adiponectin on lipopolysaccharide (LPS) plus palmitic acid (PA)-induced THP-1 cells and to identify the underlying mechanism. We report here that adiponectin was able to inhibit interleukin (IL)-1β and IL-18 by suppressing NLRP3 inflammasome activation. Furthermore, we, for the first time, describe that adiponectin attenuates NLRP3 inflammasome activation by modulating the AMPK-ROS signaling pathway. These findings provide insight suggesting that adiponectin and NLRP3 inflammasome be considered molecular targets for the development of new treatment for T2D and the related metabolic diseases. IJCEP