有氧运动对CSD引起的大鼠IR的影响  

Effect of aerobic exercise on insulin resistance induced by chronic sleep deprivation in rats

作　　者：顾兰馨 王志法[2,3] 殷强[2] 王云雅[4] 

机构地区：[1]西安市高新第一中学,陕西西安710075 [2]第四军医大学西京医院心脏外科,陕西西安710032 [3]第四军医大学生理学教研室,陕西西安710032 [4]第四军医大学西京医院核医学科,陕西西安710032

出　　处：《心脏杂志》2017年第6期652-658,共7页Chinese Heart Journal

基　　金：国家自然科学基金项目资助(81370352)

摘　　要：目的观察有氧运动对慢性睡眠剥夺(CSD)引发胰岛素抵抗(IR)的影响,并明确其可能机制。方法采用改良多平台水环境睡眠剥夺法(MMPM)对大鼠进行为期8周的睡眠剥夺建立CSD模型。雄性Sprague-Dawley大鼠30只,随机分为5组:对照组、睡眠剥夺组、睡眠剥夺+低强度运动组、睡眠剥夺+中强度运动组、睡眠剥夺+高强度运动组。通过测定空腹血清胰岛素、空腹血糖、胰岛素抵抗指数(homeostasis model assessment for insulin resistance,HOMA-IR)、心肌葡萄糖摄取、腹腔糖耐量和空腹胰岛素敏感性等手段观察有氧运动对CSD引发大鼠IR的影响;采用彩色多普勒超声诊断仪检测短轴缩短率(Fractional Shortening,FS)及左心室射血分数(Left Ventricular Ejection Fraction,LVEF);采用放射免疫法测量血清中肿瘤坏死因子(tumor necrosis factor,TNF)-α、白介素(interleukin,IL)-1β、IL-6水平;通过Western blot法检测外周血单核细胞核因子(NF-kappa B,NF-κB)以及抑制蛋白(I-kappa B,I-κB),观察有氧运动对慢性睡眠剥大鼠体内炎症因子水平及心功能的影响。结果 CSD可引起大鼠HOMA-IR、腹腔糖耐量和胰岛素敏感性的明显异常,降低心肌葡萄糖摄取和心脏功能,同时可降低抑炎因子I-κB水平,增加促炎因子NF-κB和血浆炎症因子水平(P<0.05)。低强度运动干预对上述各指标无明显影响;而中强度运动干预则可明显改善大鼠机体IR、心肌IR及心脏射血功能,增加抑炎因子I-κB,降低机体促炎因子NF-κB以及外周各炎症因子的水平(P<0.05);但高强度运动干预则可引起机体IR加重、心肌葡萄糖摄取能力下降及心脏射血分数下降,体内促炎因子NF-κB以及外周各炎症因子水平升高,而抑炎因子I-κB表达水平下降(P<0.05)。结论适量有氧运动可以通过降低体内炎症反应改善大鼠睡眠剥夺引发的IR及心功能下降。AIM To explore the effect of aerobic exercise on insulin resistance induced by sleep deprivation and the underlying mechanisms. METHODS A modified multiple platform method was used in a chronic sleep deprivation （CSD） model in rats. Thirty male 8-week-old Sprague-Dawley rats were randomized into acontrol group, CSD group, CSD with low-intensity aerobic exercise training （CSD ＋ L） group, CSD with moderate intensity exercise training （CSD ＋ M） group and CSD with high-intensity exercise training （CSD ＋ H） group （n = 6 per group）. The intraperitoneal glucose tolerance test （IPGTF）, insulin tolerance test （ITY）, positron emission tomography （PET-CT） and insulin resistance index （HOMA-IR） were employed and the levels of IL-113, IL-6, TNF-c~ and I-kappa B （I-KB） and NF-kappa B （NF-KB） in peripheral blood mononuclear cells （PBMCs） were assessed. Shortening fraction （FS） and left ventricular ejection fraction （LVEF） were measured by echocardiography after 8-week chronic sleep deprivation in all the groups with or without exercise. RESULTS Compared with those in the control group, CSD decreased HOMA-IR, insulin sensitivity and glucose tolerance as well as peripheral inflammation inhibitory cytokine （IK-B）, reduced myocardial 18FDG uptake and LVEF but increased proinflammatory cytokine NF-KB. Compared with those in the CSD group, CSD ＋ L resulted in no significant changes in the above indexes. CSD ＋ M markedly lowered CSD induced insulin resistance, decreased the level of peripheral inflammatory cytokines and proinflammatory cytokine NF-KB and increased and myocardial 18FDG uptake and LVEF. CSD ＋ H increased insulin resistance, serum inflammatory cytokines and proinflammatory cytokine NF-KB and decreased peripheral inflammation inhibitory cytokine In-B, myocardial 18FDG uptake and LVEF. CONCLUSION CSD induced significant insulin resistance and systematic inflammation; however, moderate, not low or high, intensity aerobic exercise of aerobic exercise, im

关 键 词：CSD IR 有氧运动 炎症因子 大鼠 

分 类 号：R359.2[医药卫生—基础医学]