The Role of the NLRP3 in Type 2 Diabetes–Related Inflammation and the Regulatory Impact of Exercise Interventions

Type 2 diabetes mellitus (T2DM) is a widespread metabolic disorder with a rising global prevalence and is often accompanied by various complications. Chronic inflammation plays a central role in the development and progression of T2DM, with the NLRP3 inflammasome serving as a critical regulator. This inflammasome promotes the release of pro-inflammatory cytokines and induces pyroptotic cell death through caspase-1 activation. In recent years, exercise has emerged as an effective non-pharmacological approach to managing T2DM, partly by inhibiting NLRP3 inflammasome activity and alleviating diabetes-related complications. Various forms of exercise—including aerobic training, resistance training, combined modalities, and high-intensity interval training—can modulate the NLRP3 inflammasome through diverse biological pathways. These interventions help reduce inflammation, enhance metabolic function, and provide systemic protective effects. This review outlines the structure and activation mechanisms of the NLRP3 inflammasome and comprehensively examines how different exercise modalities influence its regulation. The findings offer valuable insights and scientific support for incorporating exercise into the prevention and management strategies for T2DM.