Temporal Transcriptome Analysis of Pancreatic β-Cells in Response to Lipotoxicity and Glucolipotoxicity.

The pancreatic beta cell function failure is the core event of type 2 diabetes mellitus. High levels of free fatty acid and glucose are two main factor that induced pancreatic beta cell function failure. Long term exposure to palmitate can induced pancreatic beta cell apoptoss and impaired insulin secretion in vivo and in vitro, called lipotoxicity. The lipotoxicity often coupled with high glucose, their combination form called glucolipotoxcity. We carried out temporal transcriptome and proteome studies investigating the evolution of molecular events in Ins1 cells stimulated by palmitate for different times. And through compared the transcriptome and proteome between lipotoxicity and glucolipotoxicity explain the mechanism of glucolipotoxicity more harmfull to beta cell.胰腺β细胞功能衰竭是2型糖尿病的核心病理事件。高水平游离脂肪酸（free fatty acid）与葡萄糖是诱导胰腺β细胞功能衰竭的两大主要诱因。长期暴露于棕榈酸（palmitate）可在体内外诱导胰腺β细胞凋亡并损伤胰岛素分泌功能，该效应被称为脂毒性（lipotoxicity）。脂毒性常与高血糖协同作用，二者的联合作用模式被称为糖脂毒性（glucolipotoxicity）。本研究针对经不同时长棕榈酸刺激的Ins1细胞开展时序转录组（transcriptome）与蛋白质组（proteome）研究，以探究其分子事件的动态演化过程；并通过对比脂毒性与糖脂毒性状态下的转录组和蛋白质组差异，阐明糖脂毒性对β细胞具有更强损伤作用的分子机制。