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Volume 271, Number 43, Issue of October 25, 1996 pp. 26561-26568
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

Gq-coupled Receptors Transmit the Signal for GLUT4 Translocation via an Insulin-independent Pathway

(Received for publication, May 30, 1996, and in revised form, August 5, 1996)

Kazuhiro Kishi , Hideki Hayashi , Lihong Wang , Seika Kamohara , Keisuke Tamaoka § , Takao Shimizu , Fumitaka Ushikubi par , Shuh Narumiya par and Yousuke Ebina

From the Department of Enzyme Genetics, Institute for Enzyme Research, The University of Tokushima, 3-18-15 Kuramoto-cho, Tokushima 770, § Aoba-oka-Hospital, 14 Aoba-oka, Tondabayashi, Osaka 584,  Department of Biochemistry, Faculty of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, and the par  Department of Pharmacology, Faculty of Medicine, Kyoto University, Kyoto 606, Japan

Guanosine 5'-O-(3-thiotriphosphate) (GTPgamma S) induces the translocation of glucose transporter type 4 (GLUT4) from an intracellular pool to the cell surface and increases glucose uptake in adipocytes. The GTP-binding protein(s) responsible for the translocation has remained to be identified. Using a sensitive and quantitative method to assess the translocation of c-MYC epitope-tagged GLUT4, we obtained evidence that the activation of receptor-coupled Gq (neither Gi nor Gs) triggered GLUT4 translocation in cells, independently of insulin signaling pathway(s). Platelet-activating factor (PAF) induced GLUT4 translocation in the cells expressing the Gi- and Gq-coupled PAF receptor, but the translocation was induced even after pretreatment with wortmannin, an islet-activating protein and phorbol 12,13-dibutyrate. Norepinephrine triggered GLUT4 translocation in cells expressing the Gq-coupled alpha 1-adrenergic receptor, but prostaglandin E2 did not cause GLUT4 translocation in cells expressing the Gs-coupled EP4 receptor or the Gi-coupled EP3alpha receptor. The norepinephrine-stimulated GLUT4 translocation and glucose uptake via Gq may possibly contribute to the fuel supply required for thermogenesis in brown adipocytes and for the enhanced contractility in cardiomyocytes, both of which have an abundant endogenous GLUT4.


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