Lund S, Pryor P R, Ostergaard S, Schmitz O, Pedersen O, Holman G D
Aarhus Kommunehospital and Medical Department M (Endocrinology and Diabetes), Kommunehospitalet, Aarhus University Hospital, Denmark.
FEBS Lett. 1998 Apr 3;425(3):472-4. doi: 10.1016/s0014-5793(98)00293-2.
Both insulin and muscle contraction stimulate glucose transport activity. However, contraction stimulation does not involve the insulin signalling intermediate phosphatidylinositol 3-kinase (PI 3-kinase). Protein kinase B (PKB) has recently been identified as a direct downstream target of PI 3-kinase in the insulin signalling pathway. We have examined here whether the two stimuli share PKB as a convergent step in separate signalling pathways. Insulin stimulates both glucose transport, GLUT4 cell-surface content and PKB activity (by 4-6-fold above basal) in a wortmannin-sensitive manner in in vitro incubated rat soleus muscles. By contrast, muscle contraction, which stimulates glucose transport and the cell surface content of GLUT4 by 3-fold above basal levels, had no effect on PKB activity. These data demonstrate that PKB is not a mediator of contraction-induced glucose transport and GLUT4 translocation.
胰岛素和肌肉收缩均能刺激葡萄糖转运活性。然而，收缩刺激并不涉及胰岛素信号转导中间体磷脂酰肌醇3激酶（PI 3激酶）。蛋白激酶B（PKB）最近被确定为胰岛素信号通路中PI 3激酶的直接下游靶点。我们在此研究了这两种刺激是否在不同的信号通路中共享PKB作为一个汇聚步骤。在体外孵育的大鼠比目鱼肌中，胰岛素以渥曼青霉素敏感的方式刺激葡萄糖转运、GLUT4细胞表面含量和PKB活性（比基础水平高4至6倍）。相比之下，肌肉收缩使葡萄糖转运和GLUT4细胞表面含量比基础水平提高了3倍，但对PKB活性没有影响。这些数据表明，PKB不是收缩诱导的葡萄糖转运和GLUT4易位的介质。
