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.
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