摘要
新近发现环磷酸腺苷反应元件结合蛋白(CREB)辅激活物(TORC2)是启动糖异生的关键调控因子。空腹状态下,胰升糖素使TORC2去磷酸化,进入核内与CREB结合启动糖异生相关基因的转录。TORC2的磷酸化与去磷酸化是决定糖异生基因启动的关键环节。因此,抑制TORC2的脱磷酸或进入核内,可以减少肝糖生成,从而有望使2型糖尿病得到有效治疗。
In recent studies, the cyclic AMP-responsible element (CREB) coactivator (TORC2) has been found to stimulate the transcription of gluconeogenic genes. After dephosphorylation by glucagons during fasting, TORC2 binds with CREB to switch on gluconeogenesis in cell nucleus. The phosphorylation and dephosphorylation of TORC2 decide the stimulation of gluconeogenic gene, so inhibit the dephosphorylation of TORC2 or its entry into the nucleus can decrease the production of glycogen, which makes for effective curation of type 2 diabetes.
出处
《国际内分泌代谢杂志》
2007年第5期329-331,共3页
International Journal of Endocrinology and Metabolism