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Inhibition of cytohesins by SecinH3 leads to hepatic insulin resistance

Author

Listed:
  • Markus Hafner

    (University of Bonn
    University of Bonn)

  • Anton Schmitz

    (University of Bonn
    University of Bonn)

  • Imke Grüne

    (University of Bonn
    University of Bonn)

  • Seergazhi G. Srivatsan

    (University of Bonn
    University of Bonn)

  • Bianca Paul

    (University of Bonn)

  • Waldemar Kolanus

    (University of Bonn)

  • Thomas Quast

    (University of Bonn)

  • Elisabeth Kremmer

    (Institut für Molekulare Immunologie, GSF-Forschungszentrum für Umwelt und Gesundheit)

  • Inga Bauer

    (University of Bonn
    University of Bonn)

  • Michael Famulok

    (University of Bonn
    University of Bonn)

Abstract

Cytohesins and insulin Insulin resistance syndrome, a condition in which various organs respond insufficiently to insulin, is a major risk factor for the development of type 2 diabetes. For the majority of affected individuals, the underlying molecular defects are unknown. Hafner et al. now show that chemical inhibition of cytohesins, regulatory proteins not previously implicated in insulin-regulated metabolism, induces hepatic insulin resistance in mice. This points to impaired cytohesin function as a possible cause for insulin resistance and to cytohesin activators as a treatment for this disease. In a separate study the Drosophila cytohesin equivalent Steppke is shown to be an essential component of insulin signalling. Taken together, the two papers provide independent evidence for the involvement of cytohesins in the insulin pathway and demonstrate that the cytohesin-mediated control of this pathway is at least 800 million years old.

Suggested Citation

  • Markus Hafner & Anton Schmitz & Imke Grüne & Seergazhi G. Srivatsan & Bianca Paul & Waldemar Kolanus & Thomas Quast & Elisabeth Kremmer & Inga Bauer & Michael Famulok, 2006. "Inhibition of cytohesins by SecinH3 leads to hepatic insulin resistance," Nature, Nature, vol. 444(7121), pages 941-944, December.
    • Handle: RePEc:nat:nature:v:444:y:2006:i:7121:d:10.1038_nature05415
    DOI: 10.1038/nature05415
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