Potential role of 3‐phosphoinositide‐dependent protein kinase 1 (PDK1) in insulin‐stimulated glucose transporter 4 translocation in adipocytes

FEBS Letters

Tanti, Jean-François¹  Le Marchand-Brustel, Yannick¹  Grémeaux, Thierry¹  Grillo, Sophie¹ 

[1] Institut National de la Santé et de la Recherche Médicale, INSERM E9911 and INSERM U 145, Faculté de Médecine, Avenue de Valombrose, 06107 Nice Cedex 02, France

关键词: Insulin effect;    Okadaic acid;    Glut 4 translocation;    Adipocyte;    3-Phosphoinositide-dependent protein kinase 1;    PDK1;    3-phosphoinositide-dependent protein kinase 1;    PH;    pleckstrin homology;    PtdIns;    phosphatidylinositol;   

DOI  :  10.1016/S0014-5793(99)01472-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Insulin stimulation of Glut 4 translocation requires the activation of phosphatidylinositol 3-kinase (PI 3-kinase) but the downstream pathway remains ill-defined. We demonstrated that the overexpression of PDK1 (3-phosphoinositide-dependent protein kinase 1), a downstream effector of PI 3-kinase, stimulated Glut 4 translocation in adipocytes. This effect does not require the PH domain of PDK1, but expression of the pleckstrin homology domain-deleted PDK1 inhibits the effect of insulin, but not okadaic acid, on Glut 4 translocation. These results support a role of the PDK1 pathway in the transmission of insulin signal to Glut translocation.

【 授权许可】

Unknown