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Activation of phosphoinositide 3-kinase (PI-3K) is essential for insulin-stimulated translocation ofGLUT4and glucose transport in insulin target tissues. A novel p110γ PI-3K was reported to be activated by G i -coupled receptors via Gβγ subunits. We asked whether the stimulation of G i -coupled receptors would trigger GLUT4 translocation and glucose uptake by the activation of Gβγ-dependent p110γ PI-3K. We find that this translocation and glucose uptake can be induced by the ligand stimulation of G i -coupled α #A adrenergic receptor and fMet-Leu-Phe receptor in cells stably expressing these receptors. The noradrenaline (‘noradrenaline ’)and fMet-Leu-Phe-stimulated GLUT4 translocations were abolished by pretreatment with pertussis toxin. Pretreatment with wortmannin or genistein also inhibited the G i mediated GLUT4 translocation. On ligand stimulation of these two kinds of G i -coupled receptor, although there was a slight increase in PtdIns(3,4,5)P $ production, activation of either the p85}p110α PI-3K or Gβγ-dependent p110γ PI-3K was not

Gi-mediated translocation of GLUT4 is independent of p85/p110α and p110γ phosphoinositide 3-kinases but might involve the activation of Akt kinase