胃轻瘫是糖尿病常见的并发症之一。研究表明，自噬与凋亡参与细胞的多种生理和病理过程，且二者存在一定的联系。我们前期发现，糖尿病胃轻瘫发病过程中胃平滑肌细胞存在自噬与凋亡，且均随病程延长而加强。AMPK-mTORC1已被证实参与细胞自噬与凋亡的发生，且该通路可受高糖诱导而活化，但是具体的作用机制至今尚不清楚。基于AMPK-mTORC1将糖尿病胃轻瘫与自噬、凋亡联合进行研究，尚未见文献报道。本研究拟利用流式细胞技术、激光共聚焦显微镜技术、免疫沉淀、细胞转染、RNA干扰及Western Blot等多学科实验技术，以糖尿病大鼠模型、体外培养胃平滑肌细胞为研究对象，探讨高糖诱导自噬和凋亡在糖尿病胃轻瘫发生中的作用机制，高糖通过AMPK途径调控mTORC1的机制以及两者对自噬和凋亡的影响；本项目的研究对于进一步阐明糖尿病胃轻瘫的发病机理具有重要的理论意义，也对临床糖尿病胃轻瘫的防治具有潜在的应用价值。

Gastroparesis is one of diabetes complications. It had been shown that autophagy and apoptosis in a variety of physiological and pathological processes of the cell, and there was a certain link between the two. We previously had found that the one pathogenesis of diabetic gastroparesis was gastric smooth muscle cells in the presence of autophagy and apoptosis, and they were strengthened with the extension of the course. AMPK-mTORC1 had been shown to participate the cell autophagy and apoptosis, and the pathway was activated by high glucose-induced, but the specific mechanism of action was still unclear. It has not been reported of the literature to associate AMPK-mTORC1 pathway with autophagy with apoptosis in diabetic gastroparesis occurrence. The program will use the way of flow cytometry, confocal laser scanning microscopy, immunoprecipitation, cell transfection, RNA interference and Western Blot and other multidisciplinary experimental techniques to study diabetic rats, gastric smooth muscle cells in vitro, to explore high glucose-induced autophagy and apoptosis mechanisms occur in diabetic gastroparesis, high- glucose regulating mechanism through AMPK pathway mTORC1 and the impact of both autophagy and apoptosis. The research for this project further clarify diabetic gastroparesis pathogenesis has important theoretical significance, but also has potential applications in clinical diabetes prevention and treatment of gastroparesis.