胰岛β细胞功能受损是糖尿病(DM)发病的关键环节，保护胰岛β细胞是研究的热点和难点。健脾清热法是DM的主要治法。前期研究发现健脾消渴方改善胰岛β细胞功能与AMPK/mTORC1/SAD-A 信号通路有关。为进一步探讨健脾消渴方通过该信号通路改善胰岛β细胞的机制，体内和体外实验相结合方法，mTORC1双向调节AMPK和SAD-A活性，是信号通路的关键靶位，故体内和体外均激活或阻断mTORC1。体内实验建立T2DM大鼠模型，导入激活mTORC1重组腺病毒，健脾消渴方干预后，应用ELISA、Western Blot和RT-PCR等方法，观察该通路磷酸化及非磷酸化细胞因子蛋白量和mRNA表达的改变，及对胰岛β细胞的影响。体外实验激活和阻断mTORC1，观察健脾消渴方含药血清对高糖刺激胰岛β细胞及信号通路细胞因子蛋白量和mRNA表达的影响，明确健脾消渴方改善DM胰岛β细胞功能的作用靶点和分子机制。

Islet β-cell dysfunction is a key factor in the pathogenesis of diabetes mellitus (DM). The protection of islet βcells has been a hot and difficult field of endocrine. The invigorating spleen and resolving turbidity is the main method of treatment of diabetes. Our previous study revealed that the effect of Jianpixiaoke recipe improved islet β cell function associated with AMPK/mTORC1/SAD-A signaling pathway. To further explore the mechanism of Jianpixiaoke recipe improving the function of islet β cells by the signaling pathway, this study will apply the combination vivo with vitro methods. Because mTORC1 as the key target in the signal pathway impacts the activity of AMPK and SAD-A through a positive and negative regulator. In vivo and vitro study, activating or blocking the key target mTORC1, point to point analysis the targets for jianpixiaoke recipe. In vivo experiments the T2DM model rats were established, then injected Activated mTORC1 adenovirus via tail veins. After intervention of Jianpixiaoke recipe, methods of enzyme-linked immunosorbent assay, Western Blot and RT-PCR were applied to observe the influence of Jianpixiaoke recipe on islet βcell function, and phosphorylation and non-phosphorylated cytokine protein, the expression of mRNA in the AMPK/mTORC1/SAD-A signaling pathway. In vitro experiment analyzes molecular mechanism of Jianpixiaoke recipe by activating and blocking mTORC1, observing the effect of Jianpixiaoke recipe on islet β cell with high sugar irritation, and analyzing the mechanism of changing of differences in protein mass spectrometry. The study illustrates the influence of Jianpixiaoke recipe on the improvement of islet β cell by AMPK/mTORC1/SAD-A signaling pathway, and the mechanism of molecular and the effect of target of Jianpixiaoke recipe.