Insulin Signaling Diverges into Akt-dependent and -independent Signals to Regulate the Recruitment/Docking and the Fusion of GLUT4 Vesicles to the Plasma Membrane

摘要: Insulin modulates glucose disposal in muscle and adipose tissue by regulating the cellular redistribution of GLUT4 transporter. Protein kinase Akt/PKB is a central mediator insulin-regulated translocation GLUT4; however, trafficking step(s) regulated Akt not known. Here, we use acute pharmacological inhibition to show that required for insulin-stimulated exocytosis plasma membrane. Our data also suggest AS160 Rab GAP only target translocation. Using total internal reflection microscopy assay, activity specifically an insulin-mediated prefusion step involving recruitment and/or docking vesicles within 250 nm Moreover, fusion with membrane can occur independently activity, although based on wortmannin, it dependent phosphatidylinositol 3' activity. Hence, achieve full into membrane, insulin signaling bifurcates regulate both step(s).