NLRP3 and Glucose intolerance: In addition to serving as the essential regulator of inflammatory cell death (pyroptosis), the deficiencies of either caspase-1 or inflammasome components such as NLRP3 and apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) protected from high fat diet-induced insulin resistance, glucose intolerance, obesity [34], triglyceride metabolism [35], mitochondrial autophagy [36], and metabolic inflammation [37].