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The NLRP3 inflammasome: a sensor for metabolic danger?
Interleukin-1beta (IL-1beta), reactive oxygen species (ROS), and thioredoxin-interacting protein (TXNIP) are all implicated in the pathogenesis of type 2 diabetes mellitus (T2DM). Here we review mechanisms directing IL-1beta production and its pathogenic role in islet dysfunction during chronic hyperglycemia. In doing so, we integrate previously disparate disease-driving mechanisms for IL-1beta, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role. The NLRP3 inflammasome also drives IL-1beta maturation and secretion in another disease of metabolic dysregulation, gout. Thus, we propose that the NLRP3 inflammasome contributes to the pathogenesis of T2DM and gout by functioning as a sensor for metabolic stress.
Animals, Carrier Proteins/metabolism, Diabetes Mellitus, Type 2/immunology, Diabetes Mellitus, Type 2/metabolism, Gout/immunology, Gout/metabolism, Humans, Inflammation, Insulin-Secreting Cells/physiology, Interleukin-1beta/metabolism, Interleukin-1beta/secretion, Multiprotein Complexes/metabolism, Reactive Oxygen Species/metabolism, Stress, Physiological
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