Luttrell L M, Hewlett E L, Romero G, Rogol A D
Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908.
J Biol Chem. 1988 May 5;263(13):6134-41.
The effects of pertussis toxin (PT) treatment on insulin-stimulated myristoyl-diacylglycerol (DAG) generation, hexose transport, and thymidine incorporation were studied in differentiated BC3H-1 myocytes. Insulin treatment caused a biphasic increase in myristoyl-DAG production which was abolished in myocytes treated with PT. There was no effect of PT treatment on basal (nonstimulated) myristoyl-DAG production. Insulin-stimulated hydrolysis of a membrane phosphatidylinositol glycan was blocked by PT treatment. ADP-ribosylation of BC3H-1 plasma membranes with [32P]NAD revealed a 40-kDa protein as the major PT substrate in vivo and in vitro. The time course and dose dependence of the effects of PT on diacylglycerol generation correlated with the in vivo ADP-ribosylation of the 40-kDa substrate. Pertussis toxin treatment resulted in a 71% attenuation of insulin-stimulated hexose uptake without effect on either basal or phorbol ester-stimulated uptake. The stimulatory effects of insulin and fetal calf serum on [3H]thymidine incorporation into quiescent myocytes were attenuated by 61 and 59%, respectively, when PT was added coincidently with the growth factors. Nonstimulated and EGF-stimulated [3H]thymidine incorporation was unaffected by PT treatment. These data suggest that a PT-sensitive G protein is involved in the cellular signaling mechanisms of insulin.
在分化的BC3H-1肌细胞中研究了百日咳毒素(PT)处理对胰岛素刺激的肉豆蔻酰二酰甘油(DAG)生成、己糖转运和胸苷掺入的影响。胰岛素处理导致肉豆蔻酰-DAG生成呈双相增加,而在用PT处理的肌细胞中这种增加被消除。PT处理对基础(未刺激)的肉豆蔻酰-DAG生成没有影响。PT处理可阻断胰岛素刺激的膜磷脂酰肌醇聚糖水解。用[32P]NAD对BC3H-1质膜进行ADP核糖基化显示,一种40 kDa的蛋白质是体内和体外主要的PT底物。PT对二酰甘油生成的影响的时间进程和剂量依赖性与40 kDa底物的体内ADP核糖基化相关。百日咳毒素处理导致胰岛素刺激的己糖摄取减少71%,而对基础或佛波酯刺激的摄取均无影响。当PT与生长因子同时添加时,胰岛素和胎牛血清对静止肌细胞中[3H]胸苷掺入的刺激作用分别减弱了61%和59%。未刺激和EGF刺激的[3H]胸苷掺入不受PT处理的影响。这些数据表明,一种对PT敏感的G蛋白参与了胰岛素的细胞信号传导机制。