Tanti J F, Grillo S, Grémeaux T, Coffer P J, Van Obberghen E, Le Marchand-Brustel Y
INSERM U 145, Faculté de Médecine, Nice, France.
Endocrinology. 1997 May;138(5):2005-10. doi: 10.1210/endo.138.5.5136.
Phosphatidylinositol 3-kinase (PI 3-kinase) activation promotes glucose transporter 4 (Glut 4) translocation in adipocytes. In this study, we demonstrate that protein kinase B, a serine/threonine kinase stimulated by PI 3-kinase, is activated by both insulin and okadaic acid in isolated adipocytes, in parallel with their effects on Glut 4 translocation. In 3T3-L1 adipocytes, platelet-derived growth factor activated PI 3-kinase as efficiently as insulin but was only half as potent as insulin in promoting protein kinase B (PKB) activation. To look for a potential role of PKB in Glut 4 translocation, adipocytes were transfected with a constitutively active PKB (Gag-PKB) together with an epitope tagged transporter (Glut 4 myc). Gag-PKB was associated with all membrane fractions, whereas the endogenous PKB was mostly cytosolic. Expression of Gag-PKB led to an increase in Glut 4 myc amount at the cell surface. Our results suggest that PKB could play a role in promoting Glut 4 appearance at the cell surface following exposure of adipocytes to insulin and okadaic acid stimulation.
磷脂酰肌醇3激酶（PI 3激酶）的激活促进脂肪细胞中葡萄糖转运蛋白4（Glut 4）的转位。在本研究中，我们证明，蛋白激酶B（一种受PI 3激酶刺激的丝氨酸/苏氨酸激酶）在分离的脂肪细胞中被胰岛素和冈田酸激活，同时伴随着它们对Glut 4转位的影响。在3T3-L1脂肪细胞中，血小板衍生生长因子激活PI 3激酶的效率与胰岛素相同，但在促进蛋白激酶B（PKB）激活方面的效力仅为胰岛素的一半。为了寻找PKB在Glut 4转位中的潜在作用，将组成型活性PKB（Gag-PKB）与表位标记的转运蛋白（Glut 4 myc）一起转染到脂肪细胞中。Gag-PKB与所有膜组分相关，而内源性PKB主要位于胞质溶胶中。Gag-PKB的表达导致细胞表面Glut 4 myc量增加。我们的结果表明，PKB可能在脂肪细胞暴露于胰岛素和冈田酸刺激后促进Glut 4出现在细胞表面中发挥作用。
