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Research Article Free access | 10.1172/JCI114883

Reduced beta-cell glucose transporter in new onset diabetic BB rats.

L Orci, R H Unger, M Ravazzola, A Ogawa, I Komiya, D Baetens, H F Lodish, and B Thorens

Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Gifford Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

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Published November 1, 1990 - More info

Published in Volume 86, Issue 5 on November 1, 1990
J Clin Invest. 1990;86(5):1615–1622. https://doi.org/10.1172/JCI114883.
© 1990 The American Society for Clinical Investigation
Published November 1, 1990 - Version history
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Abstract

Previous studies from our laboratories have suggested a defect in glucose transport in islets isolated from BB rats on the first day of overt diabetes. To quantitate by immunostaining the glucose transporter of beta-cells (GLUT-2) before and at the onset of autoimmune diabetes we employed an antibody to its COOH-terminal octapeptide. On the first day of overt diabetes, defined as the day the daily blood glucose first reached 200 mg/dl, the volume density ratio of GLUT-2-positive to insulin-positive beta-cells was only 0.48 +/- 0.06, compared to 0.91 +/- 0.02 in age-matched nondiabetic diabetes-resistant controls (P less than 0.001). In age-matched nondiabetic diabetes-prone rats, most of which would have become diabetic, the ratio was 0.85 +/- 0.02, also less than the controls (P less than 0.05). Protein A-gold labeling of GLUT-2 in beta-cells of day 1 diabetic rats revealed 2.17 +/- 0.16 gold particles per micrometer length of microvillar plasma membranes compared to 3.91 +/- 0.14 in controls (P less than 0.001) and 2.87 +/- 0.24 in the nondiabetic diabetes-prone rats (P less than 0.02). Reduction in GLUT-2 correlates temporally with and may contribute to the loss of glucose-stimulated insulin secretion that precedes profound beta-cell depletion of autoimmune diabetes.

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