Evidence against protein kinase B as a mediator of contraction‐induced glucose transport and GLUT4 translocation in rat skeletal muscle

Abstract

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.