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

FEBS Letters

Holman, G.D²  Pedersen, O³  Østergaard, S¹  Pryor, P.R²  Lund, S¹  Schmitz, O¹ 

[1] Medical Research Laboratory, Aarhus Kommunehospital and Medical Department M (Endocrinology and Diabetes), Kommunehospitalet, Aarhus University Hospital, 8000 Aarhus C, Denmark;Department of Biology and Biochemistry, University of Bath, Claverton Down, Bath BA2 7AY, UK;Steno Diabetes Center and Hagedorn Research Institute, 2820 Gentofte, Copenhagen, Denmark

关键词: Protein kinase B;    Skeletal muscle;    Contraction signalling;    2-N-4-(1-Azi-2;    2;    2-trifluoroethyl)benzoyl-1;    3-bis-(d-mannos-4-yloxy)-2-propylamine;    GLUT4;   

DOI  :  10.1016/S0014-5793(98)00293-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown