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Studies on the pathogenesis of NIDDM in the GK (Goto-Kakizaki) rat

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Lessons from Animal Diabetes VI

Part of the book series: Rev.Ser.Advs.Research Diab.Animals (Birkhäuser) ((RSARDA,volume 6))

Abstract

NIDDM has a hereditary background and mainly develops on the basis of defective insulin secretion and insulin resistance in liver and extrahepatic tissues.1,2 It is still a matter of debate as to which of these defects is primary. However, impaired insulin secretion seems to be a prerequisite for the development of NIDDM.3,4 When the B-cells fail to secrete enough insulin to compensate for insulin resistance, hyperglycemia develops. In contrast, subjects with intact B-cell secretory function can handle major insulin resistance and maintain normo-glycemia by increasing their insulin secretion.

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Author information

Authors and Affiliations

  1. Department of Molecular Medicine, Endocrine and Diabetes Unit, Karolinska Institute and Hospital, Stockholm, Sweden

    Dr. Claes-Göran Östenson, Samy M. Abdel-Halim & Suad Efendic

  2. Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden

    Arne Andersson

  3. Department of Molecular Medicine, The Endocrine and Diabetes Unit, Karolinska Hospital, S-171 76, Stockholm, Sweden

    Dr. Claes-Göran Östenson

Authors
  1. Dr. Claes-Göran Östenson
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  2. Samy M. Abdel-Halim
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  3. Arne Andersson
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  4. Suad Efendic
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Editors and Affiliations

  1. Department of Biochemistry, Hadassah Medical Center, POB 12000, IL 91120, Jerusalem, Israel

    Eleazar Shafrir

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© 1996 Birkhäuser Boston

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Östenson, CG., Abdel-Halim, S.M., Andersson, A., Efendic, S. (1996). Studies on the pathogenesis of NIDDM in the GK (Goto-Kakizaki) rat. In: Shafrir, E. (eds) Lessons from Animal Diabetes VI. Rev.Ser.Advs.Research Diab.Animals (Birkhäuser), vol 6. Birkhäuser Boston. https://doi.org/10.1007/978-1-4612-4112-6_17

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  • DOI: https://doi.org/10.1007/978-1-4612-4112-6_17

  • Publisher Name: Birkhäuser Boston

  • Print ISBN: 978-1-4612-8658-5

  • Online ISBN: 978-1-4612-4112-6

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