Journal article

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

Nodi Dehvari, Dana S Hutchinson, Julia Nevzorova, Olof S Dallner, Masaaki Sato, Martina Kocan, Jon Merlin, Bronwyn A Evans, Roger J Summers, Tore Bengtsson



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..

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University of Melbourne Researchers


Awarded by NHMRC

Awarded by ARC

Funding Acknowledgements

This work was funded in part by a NHMRC Program grant 519461 (Summers). DSH is supported by a NHMRC Career Development Award (545952). MS is supported by the Wenner-Gren Foundations and ARC international fellowship (LX0989791). TB is supported by the VR-NT, VR-M from the Swedish Research Council, Novonordiskfonden, Stiftelsen Svenska Diabetesforbundets Forskningsfond, Magn. Bergvall foundation and Carl Tryggers foundation. We thank Anna Sandstrom for technical assistance.