beta 2-Adrenoceptors increase translocation of GLUT4 via GPCR kinase sites in the receptor C-terminal tail

Abstract

BACKGROUND AND PURPOSE: β-Adrenoceptor stimulation induces glucose uptake in several insulin-sensitive tissues by poorly understood mechanisms. EXPERIMENTAL APPROACH: We used a model system in CHO-K1 cells expressing the human β(2)-adrenoceptor and glucose transporter 4 (GLUT4) to investigate the signalling mechanisms involved. KEY RESULTS: In CHO-K1 cells, there was no response to β-adrenoceptor agonists. The introduction of β(2)-adrenoceptors and GLUT4 into these cells caused increased glucose uptake in response to β-adrenoceptor agonists. GLUT4 translocation occurred in response to insulin and β(2)-adrenoceptor stimulation, although the key insulin signalling intermediate PKB was not phos..