Description
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. Overall design: we performed a time-course large-scale transcriptome of INS1 cells induced by 0.5 mM palmitate and 0.5 mM palmitate with 27.8 mM glucose at four time points (8, 16, 24 and 48 h) using MAPS method