Diabetes Increases Facilitative Glucose Uptake and GLUT2 Expression at the Rat Proximal Tubule Brush Border Membrane

Authors

  • Joanne Marks,

    Corresponding author
    1. Department of Physiology, Royal Free and University College Medical School, London, UK
    2. Centre for Nephrology, Royal Free and University College Medical School, London, UK
    • Corresponding author
      J. Marks: Department of Physiology, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK. Email: marks@rfc.ucl.ac.uk

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  • Nicolas J. C. Carvou,

    1. Department of Physiology, Royal Free and University College Medical School, London, UK
    2. Centre for Nephrology, Royal Free and University College Medical School, London, UK
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  • Edward S. Debnam,

    1. Department of Physiology, Royal Free and University College Medical School, London, UK
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  • Surjit K. Srai,

    1. Department of Biochemistry and Molecular Biology, Royal Free and University College Medical School, London, UK
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  • Robert J. Unwin

    1. Department of Physiology, Royal Free and University College Medical School, London, UK
    2. Centre for Nephrology, Royal Free and University College Medical School, London, UK
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Abstract

The mechanism of renal glucose transport involves the reabsorption of filtered glucose from the proximal tubule lumen across the brush border membrane (BBM) via a sodium-dependent transporter, SGLT, and exit across the basolateral membrane via facilitative, GLUT-mediated, transport. The aim of the present study was to determine the effect of streptozotocin-induced diabetes on BBM glucose transport. We found that diabetes increased facilitative glucose transport at the BBM by 67.5 % (P < 0.05) – an effect that was abolished by overnight fasting. Western blotting and immunohistochemistry demonstrated GLUT2 expression at the BBM during diabetes, but the protein was undetectable at the BBM of control animals or diabetic animals that had been fasted overnight. Our findings indicate that streptozotocin-induced diabetes causes the insertion of GLUT2 into the BBM and this may provide a low affinity/high capacity route of entry into proximal tubule cells during hyperglycaemia.

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