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American Society for Clinical Investigation Free PMC Article

J Clin Invest. 1992 Jul;90(1):77-85. doi: 10.1172/JCI115858.

The loss of GLUT2 expression by glucose-unresponsive beta cells of db/db mice is reversible and is induced by the diabetic environment.

The Journal of clinical investigation

B Thorens, Y J Wu, J L Leahy, G C Weir

Affiliations

  1. Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142.

PMID: 1634622 PMCID: PMC443065 DOI: 10.1172/JCI115858
Free PMC Article

Abstract

Glucose-induced insulin secretion by beta cells of diabetic db/db mice was studied by a pancreas perfusion technique, and the levels of GLUT2 protein in pancreatic islets were assessed by immunofluorescence microscopy and protein blot analysis. Beta cells from diabetic mice had a high basal rate of insulin secretion; they did not respond to glucose stimulation but displayed a normal secretory response to arginine. At the same time, GLUT2 expression by db/db islets was lost whereas beta cells from nondiabetic db/+ mice expressed high levels of this transporter. GLUT2 levels in liver or kidney of diabetic mice were, however, mostly unaltered. Transplanting islets from db/db mice under the kidney capsule of db/+ mice restored normal GLUT2 levels. Conversely, transplantation of db/+ islets into db/db mice induced the disappearance of GLUT2 expression. When islets from db/+ mice were transplanted under the kidney capsule of streptozocin-diabetic mice, the immunodetection of GLUT2 also disappeared. We conclude that: (a) GLUT2 expression is decreased in glucose-unresponsive beta cells from db/db mice; (b) the decreased expression of GLUT2 is reversible; (c) the loss of GLUT2 expression is induced by the diabetic environment of db/db and streptozocin-induced diabetic mice. These observations together with previously published data suggest that a factor different from glucose or insulin regulates the beta cell expression of GLUT2.

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References

  1. Diabetes Metab Rev. 1986;2(1-2):125-61 - PubMed
  2. Cell. 1988 Oct 21;55(2):281-90 - PubMed
  3. Nucleic Acids Res. 1989 Dec 11;17(23):10099 - PubMed
  4. Proc Natl Acad Sci U S A. 1986 Dec;83(24):9749-53 - PubMed
  5. J Biol Chem. 1990 Apr 25;265(12):6548-51 - PubMed
  6. Proc Natl Acad Sci U S A. 1990 Sep;87(17):6492-6 - PubMed
  7. Proc Natl Acad Sci U S A. 1990 Jun;87(11):4088-92 - PubMed
  8. Diabetes Care. 1990 Mar;13(3):209-18 - PubMed
  9. J Clin Invest. 1990 Mar;85(3):962-7 - PubMed
  10. Diabetologia. 1983 Nov;25(5):439-43 - PubMed
  11. N Engl J Med. 1983 Feb 10;308(6):322-5 - PubMed
  12. J Histochem Cytochem. 1974 Dec;22(12):1077-83 - PubMed
  13. J Clin Invest. 1974 Dec;54(6):1403-12 - PubMed
  14. Diabetes. 1972 Apr;21(4):224-34 - PubMed
  15. J Clin Invest. 1973 Apr;52(4):870-6 - PubMed
  16. Acta Endocrinol (Copenh). 1972 Jul;70(3):487-509 - PubMed
  17. Dan Med Bull. 1972 Oct;19(7):222-6 - PubMed
  18. J Clin Endocrinol Metab. 1976 Aug;43(2):279-86 - PubMed
  19. Science. 1990 Oct 26;250(4980):546-9 - PubMed
  20. Am J Physiol. 1990 Dec;259(6 Pt 1):C279-85 - PubMed
  21. Development. 1991 Sep;113(1):363-72 - PubMed
  22. Science. 1991 Mar 8;251(4998):1200-5 - PubMed
  23. Proc Natl Acad Sci U S A. 1990 Dec;87(24):9953-7 - PubMed
  24. Am J Physiol. 1990 Dec;259(6 Pt 1):C286-94 - PubMed
  25. J Clin Invest. 1990 Nov;86(5):1615-22 - PubMed
  26. Diabetes Care. 1990 Sep;13(9):992-1010 - PubMed
  27. Science. 1989 Jul 21;245(4915):295-7 - PubMed

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