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Glycolysis regulates NLRP3 inflammasome activation in macrophages. However, how lactic acid fermentation and pyruvate oxidation controlled by the mitochondrial pyruvate carrier (MPC) affect NLRP3 inflammasome activation and autoinflammatory disease remains elusive. We found that the inactivation of MPC with genetic depletion or pharmacological inhibitors, MSDC\u20100160 or pioglitazone, increased NLRP3 inflammasome activation and IL\u20101\u03b2 secretion in macrophages. Glycolytic reprogramming induced by MPC inhibition skewed mitochondrial ATP\u2010associated oxygen consumption into cytosolic lactate production, which enhanced NLRP3 inflammasome activation in response to monosodium urate (MSU) crystals. As pioglitazone is an insulin sens MSDC\u2010itizer used for diabetes, its MPC inhibitory effect in diabetic individuals was investigated. 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