Background Exercise is an effective intervention for obesity and type 2 diabetes,with significant physiological benefits over pharmacological interventions.However,there is limited preclinical data available comparing...Background Exercise is an effective intervention for obesity and type 2 diabetes,with significant physiological benefits over pharmacological interventions.However,there is limited preclinical data available comparing endurance and resistance exercise for the impacts on obesogenic pathology and glycemic control.Methods Male mice were subjected to 8 weeks of diet-induced obesity(DIO)by high-fat diet(HFD)feeding concurrent with voluntary wheel running(endurance exercise(EEX))or weightlifting(resistance exercise(REX)).Sedentary(SED)mice fed on normal chow(NC)or HFD were used as controls.Results EEX and REX interventions significantly attenuated weight gain vs.HFD-SED due to reduction of fat mass,not changes in lean mass,as assessed by EchoMRI.While REX suppressed visceral and subcutaneous fat accumulation significantly,only EEX enlarged brown fat mass.Exercise tolerance testing(i.e.,run-to-fatigue)revealed significantly improved exercise capacity in EEX group vs.NC-SED.Interestingly,although HFD led to trends of increased skeletal muscle mass,only EEX with HFD led to significant muscle weight gain.Neither exercise modality resulted in significant changes of hindlimb skeletal muscle contractile properties and cardiac function compared to SED mice on HFD.Importantly,REX showed significantly enhanced benefits over EEX in improving homeostatic model assessment of insulin resistance(HOMA-IR),glucose tolerance,and insulin tolerance.Conclusion These results provide a direct and translatable comparison of endurance and resistance exercise training in a preclinical context of obesity and hyperglycemia.The current data set demonstrates an advantage of resistance exercise over endurance exercise in improving glucose and insulin tolerance under the condition of obesity,and that these improvements are independent of significant alterations of muscle weight gain and exercise performance.展开更多
背景:细胞焦亡作为一种典型的促炎性程序性细胞死亡方式,在先天免疫过程中发挥重要作用,其过度激活则会引发机体炎症反应与疾病的发生,例如胰岛β细胞焦亡与2型糖尿病的病理生理过程密切相关。如今越来越多的研究表明,运动可以作为一种...背景:细胞焦亡作为一种典型的促炎性程序性细胞死亡方式,在先天免疫过程中发挥重要作用,其过度激活则会引发机体炎症反应与疾病的发生,例如胰岛β细胞焦亡与2型糖尿病的病理生理过程密切相关。如今越来越多的研究表明,运动可以作为一种抑制胰岛β细胞焦亡、防治2型糖尿病及其并发症的有效措施,但现阶段胰岛β细胞焦亡、2型糖尿病及运动三者之间的潜在关系尚不明确。目的:综述细胞焦亡一系列途径,及胰岛β细胞焦亡、核苷酸结合寡聚化结构域样受体蛋白3炎症小体在2型糖尿病病理生理过程中的分子机制,并总结不同运动方式调控胰岛β细胞焦亡、防治2型糖尿病的效果与潜在机制,以期为防治2型糖尿病寻找新靶点及进行运动干预提供理论与实践指导。方法:系统检索了2000年1月至2025年4月中国知网(CNKI)、维普中文期刊服务平台、万方数据库、谷歌学术、Web of Science、PubMed收录的相关文献,筛选与运动调控细胞焦亡防治2型糖尿病相关的高质量研究。依据明确的纳入和排除标准,对文献质量进行评估与整合,最终对纳入的57篇文献进行分析与总结。结果与结论:①核苷酸结合寡聚化结构域样受体蛋白3炎症小体介导的细胞焦亡在2型糖尿病的发生发展中发挥重要作用;②多种运动干预,特别是有氧运动,可通过抑制核苷酸结合寡聚化结构域样受体蛋白3相关通路、减轻炎症反应,有效改善胰岛β细胞损伤,提升胰岛素敏感性;③太极拳与易筋经、抗阻运动及低氧运动亦展现出一定调控潜力。综上,运动通过多途径干预细胞焦亡,为防治2型糖尿病提供了新靶点的理论支撑和实践方向。展开更多
糖尿病是一种常见的代谢性疾病,其病因和病程主要与胰岛素分泌不足和胰岛素抵抗密切相关。代谢重编程是细胞在病理或应激条件下重塑代谢途径以适应能量与生物合成需求的过程。研究表明,在糖尿病中,代谢重编程可通过影响线粒体功能、糖...糖尿病是一种常见的代谢性疾病,其病因和病程主要与胰岛素分泌不足和胰岛素抵抗密切相关。代谢重编程是细胞在病理或应激条件下重塑代谢途径以适应能量与生物合成需求的过程。研究表明,在糖尿病中,代谢重编程可通过影响线粒体功能、糖酵解和脂代谢等影响胰岛素敏感性和胰岛β细胞功能。本文系统综述了代谢重编程在糖尿病发生、发展过程中的变化特征和作用机制,并重点介绍了胰岛素信号通路和单磷酸腺苷活化蛋白激酶(adenosine 5′-monophosphate-activated protein kinase,AMPK)信号通路在调控糖、脂代谢中的作用,旨在为了解糖尿病发病机制及其寻找防治、靶向干预策略提供新思路。展开更多
基金supported by National Institutes of Health(No.NIH-R01AR050429 and No.NIH-R01AR077440)a grant by Red Gates Foundation to ZY.
摘要Background Exercise is an effective intervention for obesity and type 2 diabetes,with significant physiological benefits over pharmacological interventions.However,there is limited preclinical data available comparing endurance and resistance exercise for the impacts on obesogenic pathology and glycemic control.Methods Male mice were subjected to 8 weeks of diet-induced obesity(DIO)by high-fat diet(HFD)feeding concurrent with voluntary wheel running(endurance exercise(EEX))or weightlifting(resistance exercise(REX)).Sedentary(SED)mice fed on normal chow(NC)or HFD were used as controls.Results EEX and REX interventions significantly attenuated weight gain vs.HFD-SED due to reduction of fat mass,not changes in lean mass,as assessed by EchoMRI.While REX suppressed visceral and subcutaneous fat accumulation significantly,only EEX enlarged brown fat mass.Exercise tolerance testing(i.e.,run-to-fatigue)revealed significantly improved exercise capacity in EEX group vs.NC-SED.Interestingly,although HFD led to trends of increased skeletal muscle mass,only EEX with HFD led to significant muscle weight gain.Neither exercise modality resulted in significant changes of hindlimb skeletal muscle contractile properties and cardiac function compared to SED mice on HFD.Importantly,REX showed significantly enhanced benefits over EEX in improving homeostatic model assessment of insulin resistance(HOMA-IR),glucose tolerance,and insulin tolerance.Conclusion These results provide a direct and translatable comparison of endurance and resistance exercise training in a preclinical context of obesity and hyperglycemia.The current data set demonstrates an advantage of resistance exercise over endurance exercise in improving glucose and insulin tolerance under the condition of obesity,and that these improvements are independent of significant alterations of muscle weight gain and exercise performance.
摘要背景:细胞焦亡作为一种典型的促炎性程序性细胞死亡方式,在先天免疫过程中发挥重要作用,其过度激活则会引发机体炎症反应与疾病的发生,例如胰岛β细胞焦亡与2型糖尿病的病理生理过程密切相关。如今越来越多的研究表明,运动可以作为一种抑制胰岛β细胞焦亡、防治2型糖尿病及其并发症的有效措施,但现阶段胰岛β细胞焦亡、2型糖尿病及运动三者之间的潜在关系尚不明确。目的:综述细胞焦亡一系列途径,及胰岛β细胞焦亡、核苷酸结合寡聚化结构域样受体蛋白3炎症小体在2型糖尿病病理生理过程中的分子机制,并总结不同运动方式调控胰岛β细胞焦亡、防治2型糖尿病的效果与潜在机制,以期为防治2型糖尿病寻找新靶点及进行运动干预提供理论与实践指导。方法:系统检索了2000年1月至2025年4月中国知网(CNKI)、维普中文期刊服务平台、万方数据库、谷歌学术、Web of Science、PubMed收录的相关文献,筛选与运动调控细胞焦亡防治2型糖尿病相关的高质量研究。依据明确的纳入和排除标准,对文献质量进行评估与整合,最终对纳入的57篇文献进行分析与总结。结果与结论:①核苷酸结合寡聚化结构域样受体蛋白3炎症小体介导的细胞焦亡在2型糖尿病的发生发展中发挥重要作用;②多种运动干预,特别是有氧运动,可通过抑制核苷酸结合寡聚化结构域样受体蛋白3相关通路、减轻炎症反应,有效改善胰岛β细胞损伤,提升胰岛素敏感性;③太极拳与易筋经、抗阻运动及低氧运动亦展现出一定调控潜力。综上,运动通过多途径干预细胞焦亡,为防治2型糖尿病提供了新靶点的理论支撑和实践方向。
摘要糖尿病是一种常见的代谢性疾病,其病因和病程主要与胰岛素分泌不足和胰岛素抵抗密切相关。代谢重编程是细胞在病理或应激条件下重塑代谢途径以适应能量与生物合成需求的过程。研究表明,在糖尿病中,代谢重编程可通过影响线粒体功能、糖酵解和脂代谢等影响胰岛素敏感性和胰岛β细胞功能。本文系统综述了代谢重编程在糖尿病发生、发展过程中的变化特征和作用机制,并重点介绍了胰岛素信号通路和单磷酸腺苷活化蛋白激酶(adenosine 5′-monophosphate-activated protein kinase,AMPK)信号通路在调控糖、脂代谢中的作用,旨在为了解糖尿病发病机制及其寻找防治、靶向干预策略提供新思路。