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The facilitative glucose transporter 2: pathophysiological role in mouse and human

  • Chapter
Membrane Transporter Diseases

Abstract

Glucose is an essential substrate for the metabolism of most cells. Because glucose is a polar molecule, its transport through biological membranes requires specific transporter proteins. Transport of glucose through the apical membrane of intestinal and kidney epithelial cells depends on the presence of active Na+/glucose symporters, SGLT-l and SGLT-2, which concentrate glucose inside the cells using the energy provided by cotransport of Na+ ions down their electrochemical gradient (Hediger and Rhoads 1994). Facilitated diffusion of glucose through the cellular membrane is otherwise catalyzed by glucose carriers (protein symbol GLUT, gene symbol SLC2 for Solute Carrier Family 2) that belong to a superfamily of transport facilitators which comprises organic anion and cation transporters, yeast hexose transporters, plant hexose/proton symporters, and bacterial sugar/ proton symporters (Henderson 1993).

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Author information

Authors and Affiliations

  1. Institut Cochin-INSERM U567, 24, Rue du Faubourg Saint-Jacques, 75014, Paris, France

    Marc Foretz

  2. Institute of Pharmacology and Toxicology, 27 rue du Bugnon, CH 1005, Lausanne, Switzerland

    Bernard Thorens

Authors
  1. Marc Foretz
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  2. Bernard Thorens
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Editors and Affiliations

  1. Australian National University, Canberra, Australia

    Stefan Bröer

  2. University of Zurich, Zurich, Switzerland

    Carsten A. Wagner

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© 2003 Springer Science+Business Media New York

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Foretz, M., Thorens, B. (2003). The facilitative glucose transporter 2: pathophysiological role in mouse and human. In: Bröer, S., Wagner, C.A. (eds) Membrane Transporter Diseases. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9023-5_12

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  • DOI: https://doi.org/10.1007/978-1-4419-9023-5_12

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-4761-3

  • Online ISBN: 978-1-4419-9023-5

  • eBook Packages: Springer Book Archive

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