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Obesity-induced overexpression of miR-802 impairs glucose metabolism through silencing of Hnf1b

Author

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  • Jan-Wilhelm Kornfeld

    (Max-Planck-Institute for Neurological Research, Gleueler Strasse 50a, 50931 Cologne, Germany
    Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Zülpicher Strasse 47a, 50674 Cologne, Germany
    Institute for Genetics, University of Cologne, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne and Center for Molecular Medicine Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Catherina Baitzel

    (Max-Planck-Institute for Neurological Research, Gleueler Strasse 50a, 50931 Cologne, Germany
    Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Zülpicher Strasse 47a, 50674 Cologne, Germany
    Institute for Genetics, University of Cologne, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne and Center for Molecular Medicine Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • A. Christine Könner

    (Max-Planck-Institute for Neurological Research, Gleueler Strasse 50a, 50931 Cologne, Germany
    Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Zülpicher Strasse 47a, 50674 Cologne, Germany
    Institute for Genetics, University of Cologne, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne and Center for Molecular Medicine Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Hayley T. Nicholls

    (Max-Planck-Institute for Neurological Research, Gleueler Strasse 50a, 50931 Cologne, Germany
    Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Zülpicher Strasse 47a, 50674 Cologne, Germany
    Institute for Genetics, University of Cologne, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne and Center for Molecular Medicine Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Merly C. Vogt

    (Max-Planck-Institute for Neurological Research, Gleueler Strasse 50a, 50931 Cologne, Germany
    Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Zülpicher Strasse 47a, 50674 Cologne, Germany
    Institute for Genetics, University of Cologne, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne and Center for Molecular Medicine Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Karolin Herrmanns

    (Swiss Federal Institute of Technology (ETH Zurich), Institute of Molecular Health Science, Schafmattstrasse 22, 8093 Zurich, Switzerland)

  • Ludger Scheja

    (University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany)

  • Cécile Haumaitre

    (INSERM U 969, 9 Quai Saint Bernard, 75005 Paris, France
    CNRS Université Pierre et Marie Curie UMR7622, 9 Quai Saint Bernard, 75005 Paris, France)

  • Anna M. Wolf

    (University Hospital of Ulm, Albert-Einstein-Allee 23, 89081 Ulm, Germany)

  • Uwe Knippschild

    (University Hospital of Ulm, Albert-Einstein-Allee 23, 89081 Ulm, Germany)

  • Jost Seibler

    (TaconicArtemis GmbH, Neurather Ring 1, 51063 Cologne, Germany)

  • Silvia Cereghini

    (INSERM U 969, 9 Quai Saint Bernard, 75005 Paris, France
    CNRS Université Pierre et Marie Curie UMR7622, 9 Quai Saint Bernard, 75005 Paris, France)

  • Joerg Heeren

    (University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany)

  • Markus Stoffel

    (Swiss Federal Institute of Technology (ETH Zurich), Institute of Molecular Health Science, Schafmattstrasse 22, 8093 Zurich, Switzerland)

  • Jens C. Brüning

    (Max-Planck-Institute for Neurological Research, Gleueler Strasse 50a, 50931 Cologne, Germany
    Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Zülpicher Strasse 47a, 50674 Cologne, Germany
    Institute for Genetics, University of Cologne, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne and Center for Molecular Medicine Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

Abstract

The livers of obese mice and humans show increased levels of miR-802 resulting in impaired glucose tolerance and decreased insulin sensitivity through silencing of Hnf1b, revealing a novel pathway with potential relevance for type 2 diabetes.

Suggested Citation

  • Jan-Wilhelm Kornfeld & Catherina Baitzel & A. Christine Könner & Hayley T. Nicholls & Merly C. Vogt & Karolin Herrmanns & Ludger Scheja & Cécile Haumaitre & Anna M. Wolf & Uwe Knippschild & Jost Seibl, 2013. "Obesity-induced overexpression of miR-802 impairs glucose metabolism through silencing of Hnf1b," Nature, Nature, vol. 494(7435), pages 111-115, February.
    • Handle: RePEc:nat:nature:v:494:y:2013:i:7435:d:10.1038_nature11793
    DOI: 10.1038/nature11793
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