Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

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.

This is a preview of subscription content

Access options

Buy article

Get time limited or full article access on ReadCube.

$32.00

Buy

All prices are NET prices.

References

  1. Karnielli, E., Hissin, P. J., Simpson, I. A., Salans, L. B. & Cushman, S. W. J. clin. Invest. 68, 811–814 (1981).

    Article  Google Scholar 

  2. Kahn, B. B. & Cushman, S. W. J. biol. Chem. 262, 5118–5124 (1987).

    CAS  PubMed  Google Scholar 

  3. Kahn, B. B., Simpson, I. A. & Cushman, S. W. J. clin. Invest. 82, 691–699 (1988).

    CAS  Article  Google Scholar 

  4. James, D. E., Brown, R., Navarro, J. & Pilch, P. F. Nature 333, 183–185 (1988).

    ADS  CAS  Article  Google Scholar 

  5. James, D. E., Strube, M. & Mueckler, M. Nature 338, 83–87 (1989).

    ADS  CAS  Article  Google Scholar 

  6. Birnbaum, M. J. Cell 57, 305–315 (1989).

    CAS  Article  Google Scholar 

  7. Charron, M. J., Brosius, F. C., Alper, S. L. & Lodish, H. F. Proc. natn. Acad. Sci. U.S.A. 86, 2535–2539 (1989).

    ADS  CAS  Article  Google Scholar 

  8. Fukumoto, H. et al. J. biol. Chem. 264, 7776–7779 (1989).

    CAS  PubMed  Google Scholar 

  9. Mueckler, M. et al. Science 229, 941–945 (1985).

    ADS  CAS  Article  Google Scholar 

  10. Birnbaum, M. J., Haspel, H. C. & Rosen, O. M. Proc. natn. Acad. Sci. U.S.A. 83, 5784–5788 (1986).

    ADS  CAS  Article  Google Scholar 

  11. Cushman, S. W. & Wardzala, L. J. J. biol. Chem. 255, 4758–4762 (1980).

    CAS  PubMed  Google Scholar 

  12. Suzuki, K. & Kono, T. Proc. natn. Acad. Sci. U.S.A. 77, 2542–2545 (1980).

    ADS  CAS  Article  Google Scholar 

  13. Simpson, I. A. & Cushman. S. W. A. Rev. Biochem. 55, 1059–1089 (1986).

    CAS  Article  Google Scholar 

  14. Wang, C. J. biol. Chem. 262, 15689–15695 (1987).

    CAS  PubMed  Google Scholar 

  15. Oka, Y. et al. J. biol. Chem. 263, 13432–13439 (1988).

    CAS  PubMed  Google Scholar 

  16. Zorzano, A. et al. J. biol. Chem. (in the press).

  17. Sivitz, W. I., DeSautel, S. L., Kayano, T., Bell, G. I. & Pessin, J. E. Nature 340, 72–74 (1989).

    ADS  CAS  Article  Google Scholar 

  18. Garvey, W. T., Huecksteadt, T. P., Matthaei, S. & Olefsky, J. M. J. clin. Invest. 81, 1528–1536 (1988).

    CAS  Article  Google Scholar 

  19. Rodbell, M. J. biol. Chem. 239, 375–380 (1964).

    CAS  PubMed  Google Scholar 

  20. Bradford, M. M. Analyt. Biochem. 72, 248–254 (1976).

    CAS  Article  Google Scholar 

  21. Laemmli, J. K. Nature 227, 680–685 (1970).

    ADS  CAS  Article  Google Scholar 

Download references

Author information

Author notes

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

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

Authors
  1. Joel Berger
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Chhabi Biswas
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Pasquale P. Vicario
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. H. Vincent Strout
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Richard Saperstein
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Paul F. Pilch
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and Permissions

About this article

Cite this article

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

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1038/340070a0

Further reading

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing