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Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting

Nature volume 340, pages 70–72 (1989)Cite this article

Abstract

CELLULAR resistance to insulin caused by a reduction in insulinmediated glucose uptake can be produced in rats by chemically inducing diabetes with streptozotocin and by fasting1—3. Two glucose transporter isoforms are expressed in fat cells: (1) the insulin-responsive species4—8 which is found only in fat and muscle, and (2) a species corresponding to the erythrocyte/Hep G2/rat brain transporter9,10. We show here that fat cells isolated from streptozotocin diabetic rats and from fasted rats show a significant (60—80%) decrease in the amount of immunologically detectable insulin-sensitive glucose transporter and no change in the level of the Hep G2/rat brain transporter. Administration of insulin and refeeding, respectively, result in a return of the insulin-sensitive glucose transporter to levels that are normal or slightly above normal. Thus, peripheral tissue insulin resistance could be due to the specific reduction in the amount of insulin-sensitive glucose transporter.

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Author notes

  1. Paul F. Pilch: Department of Biochemistry, Boston University School of Medicine, 80 East Concord Street, Boston, Massachusetts 02118, USA

Authors and Affiliations

  1. Department of Biochemical Endocrinology, Merck Institute for Therapeutic Research, Rahway, New Jersey, 07065, USA

    Joel Berger, Chhabi Biswas, Pasquale P. Vicario, H. Vincent Strout, Richard Saperstein & Paul F. Pilch

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  1. Joel Berger
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  2. Chhabi Biswas
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  3. Pasquale P. Vicario
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  4. H. Vincent Strout
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  5. Richard Saperstein
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  6. Paul F. Pilch
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Berger, J., Biswas, C., Vicario, P. et al. Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting. Nature 340, 70–72 (1989). https://doi.org/10.1038/340070a0

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