NLRP3炎症小体参与运动改善胰岛素抵抗的机制研究进展

Research progress on mechanism of NLRP3 inflammasome involved in exercise improve insulin resistance

NLRP3炎症小体在胰岛素抵抗(IR)中发挥关键调节作用。NLRP3炎症小体相关信号因子表达参与运动改善胰腺、脂肪组织、肝脏及骨骼肌等靶组织IR。运动可通过显著降低NLRP3炎症小体等炎症因子表达减少脂肪组织炎症和肝脏脂肪变性,提高β细胞功能及骨骼肌葡萄糖摄取能力改善2型糖尿病IR。本文主要对NLRP3炎症小体在运动改善IR的潜在分子机制进行综述,为代谢性疾病的运动干预及治疗提供参考。

NLRP3 plays a crucial regulatory role in insulin resistance(IR).NLRP3 inflammasome related signal factor expression is involved in exercise improve IR in target tissues such as pancreas,adipose tissue,liver and skeletal muscle.Exercise can reduce adipose tissue inflammation and liver steatosis,and improveβcell function and skeletal muscle glucose uptake by significantly reducing expression of NLRP3 inflammasome and other inflammatory factors,thereby improving IR in type 2 diabetes.This article reviews potential molecular mechanism of NLRP3 inflammasome in improving IR during exercise,to provide valuable reference for exercise intervention and treatment of metabolic diseases.