生长休止特异转录子5（growth-arrest-specific transcript 5，GAS5）是我们前期研究发现与胰岛β细胞功能关系密切的lncRNA：T2DM模型db/db小鼠胰岛中lncRNA GAS5表达显著性下降；lncRNA GAS5低表达导致胰岛β细胞转录抑制因子Insm1显著上调、胰岛素分泌量减少、细胞周期阻滞于G1期。研究显示，lnsm1与胰岛素基因转录和细胞周期相关。我们提出假说：lncRNA GAS5可能通过调控Insm1表达影响胰岛β细胞功能。研究拟评估lncRNA GAS5与胰岛β细胞数量、细胞周期、胰岛素合成及分泌之间的关系；应用过表达和基因沉默技术，探讨lncRNA GAS5调控胰岛β细胞功能的生物学作用；以Insm1为线索，论证lncRNA GAS5调控胰岛β细胞功能的分子机制。预期研究结果将为阐明糖尿病发病机制提供新视角，为糖尿病防治提供新靶点。

lncRNA GAS5 was found to be closely associated with pancreatic islet β cells function. Our previous studies revealed that lncRNA GAS5 expression decreased significantly in islets of T2DM animal model (db/db) mice; Low expression of lncRNA GAS5 resulted in a significant up-regulation of transcriptional inhibitory factor Insm1, decreased insulin secretion, and cell cycle arrest in G1 phase. Studies have shown that lnsm1 is associated with insulin gene transcription and cell cycle function. We hypothesized that lncRNA GAS5 may affect islet β cell function by regulating Insm1 expression. Based on our data, we will investigate the relationship between the expression of lncRNA GAS5 and the number of pancreatic β cells, cell cycle, insulin synthesis and secretion; Adopting overexpression and knock down strategies in vitro and in vivo, we intend to explicit the effect of lncRNA GAS5 on regulation of islet β cell function; Insm1 was regarded as a key clue, rescue experiments would be implemented to demonstrate the molecular mechanisms of lncRNA GAS5 in regulation of pancreatic β cell function. It is expected that the findings will help to understand the role of lncRNA in islet function failure from a novel perspective, and it may provide new intervention targets for the prevention and treatment of diabetes.