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

被引：12

作者：

Grillo, S ^{[1
]}

Grémeaux, T ^{[1
]}

Le Marchand-Brustel, Y ^{[1
]}

Tanti, JF ^{[1
]}

机构：

[1] Fac Med, INSERM, U145, F-06107 Nice 02, France

来源：

FEBS LETTERS | 1999年 / 461卷 / 03期

关键词：

insulin effect; okadaic acid; glut; 4; translocation; adipocyte; 3-phosphoinositide-dependent protein kinase 1;

D O I：

10.1016/S0014-5793(99)01472-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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. (C) 1999 Federation of European Biochemical Societies.

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页码：277 / 279

页数：3

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