胰岛素抵抗(IR)是多种代谢性疾病的共同病理生理基础。新型激素Irisin通过运动诱导其相关代谢通路，促使白色脂肪细胞转变为棕色脂肪细胞，进而发挥改善IR的功能。我们前期发现运动复合高温比单独运动或高温具有更佳的改善IR效果。本研究拟以我们前期的高脂饮食性IR大鼠模型为实验对象，通过验证7周的运动、高温、运动复合高温对高脂饮食性IR大鼠改善效果，应用Western blot、ELISA、电镜等技术，分析运动和高温对慢肌(比目鱼肌)和快肌(趾长伸肌)PGC-1α、Irisin蛋白水平的影响，观察Ca2+依赖性信号通路CaMKIV与CnA指标和p38MAPK通路指标，测试棕色脂肪蛋白标志物UCP1蛋白的变化，并应用Irisin基因敲除大鼠实验进行验证，以期探讨运动和高温对机体IR改善的Irisin代谢通路机制，为运动、高温角度提供IR改善的"绿色"方法提供理论基础。

Insulin resistance (IR) is associated with many related health complications. Previous studies demonstrated that heat and exercise could have positive function on IR separately. Novel hormone Irisin induced by exercise could have related metabolic pathways that transfer white fat cells into brown fat cells with the catabolism, furthermore play commuted IR function. Earlier our study in IR rats induced by high-fat diet showed that exercise combined with high temperature had more effective on IR. This study is based on our previous IR rats, to verify the positive effects of seven weeks exercise alone, heat alone, and exercise combined with high temperature on IR wistar rats. The methods of Western blot, ELISA, transmission electron microscope will be used in the study. Slow-twitch soleus and fast-twitch extensor digitorum longus (EDL) will be assessed for PGC-1α and Irisin protein levels. Calcineurin A (CnA) and Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) for Ca2+ dependent signaling pathway, and mitogen-activited protein kinase (p38MAPK) pathway will be measured in this study. Changes of brown fat protein markers UCP1 protein in the adipose tissue will be investigated. In addition, Irisin knock out rats will be used in this study to verify the results. We hypothesized that exercise and heat treatment would mitigate the development of IR from Irisin pathway. The study also provides potential "green" methods for therapeutic treatment of insulin resistance.

胰岛素抵抗（IR）与诸多疾病发生高度有关。以往的研究表明，单独的高温或运动干预均可以改善胰岛素抵抗，本研究的目的是为了验证运动复合高温比单独运动或高温具有更佳的改善IR效果。本研究首先构建了高脂饮食性IR大鼠模型，通过验证7周的运动、高温、运动复合高温对高脂饮食性IR大鼠改善效果，应用了Western blot、ELISA、电镜等技术，分析了运动和高温对慢肌(比目鱼肌)和快肌(趾长伸肌)PGC-1α、Irisin蛋白水平的影响，观察了Ca2+依赖性信号通路CaMKIV与CnA指标和p38MAPK通路指标，测试了棕色脂肪蛋白标志物UCP1蛋白的变化，并应用Irisin基因敲除大鼠实验进行验证。结果发现，运动复合高温可以提高血清Irisi (P < 0.05)n和棕色脂肪标志物UCP1水平(P < 0.05)，而具体机制可能从慢肌（比目鱼肌）的PGC-1a、CnA、p38MAPK相关通路表现出改善胰岛素抵抗的效果。综上结果提示，运动复合高温比单独运动或高温具有更佳的改善大鼠机体IR效果，此研究将为运动、高温角度提供IR改善的"绿色"方法提供理论基础。