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FEBS Lett. 1999 Nov 19;461(3):277-9.

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

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Institut National de la Santé et de la Recherche Médicale, INSERM E9911 and INSERM U 145, Faculté de Médecine, Avenue de Valombrose, 06107, Nice, France.


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.

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