Inhibition of cytohesins by SecinH3 leads to hepatic insulin resistance

Markus Hafner, Anton Schmitz, Imke Grüne, Seergazhi G. Srivatsan, Bianca Paul, Waldemar Kolanus, Thomas Quast, Elisabeth Kremmer, Inga Bauer and Michael Famulok ()
Additional contact information
Markus Hafner: University of Bonn
Anton Schmitz: University of Bonn
Imke Grüne: University of Bonn
Seergazhi G. Srivatsan: 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
Michael Famulok: University of Bonn

Nature, 2006, vol. 444, issue 7121, 941-944

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.

Date: 2006
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DOI: 10.1038/nature05415

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