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Fischer et al. reply

Author

Listed:
  • Julia Fischer

    (* Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany. ruether@uni-duesseldorf.de)

  • Linda Koch

    (University of Cologne
    Center of Molecular Medicine Cologne (CMMC) and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne)

  • Christian Emmerling

    (* Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany. ruether@uni-duesseldorf.de)

  • Jeanette Vierkotten

    (* Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany. ruether@uni-duesseldorf.de
    Present addresses: Department of Dermatology, Center of Molecular Medicine Cologne (CMMC), University of Cologne, D-50674 Cologne, Germany (J.V.); Epidauros Biotechnologie AG, D-82347 Bernried, Germany (T.P.))

  • Thomas Peters

    (* Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany. ruether@uni-duesseldorf.de
    Present addresses: Department of Dermatology, Center of Molecular Medicine Cologne (CMMC), University of Cologne, D-50674 Cologne, Germany (J.V.); Epidauros Biotechnologie AG, D-82347 Bernried, Germany (T.P.))

  • Jens C. Brüning

    (University of Cologne
    Center of Molecular Medicine Cologne (CMMC) and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne
    Max-Planck Institute for the Biology of Ageing)

  • Ulrich Rüther

    (* Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany. ruether@uni-duesseldorf.de)

Abstract

Replying to: J. R. Speakman Nature 464, 10.1038/nature08807 (2010) The human studies on FTO reported an association of an intronic single nucleotide polymorphism (SNP) with obesity. Our report of mice with the targeted inactivation of the Fto gene demonstrated a direct role of Fto in energy homeostasis1. We have shown that the absence of Fto protein results in leanness and that Fto deficiency affects energy homeostasis. Speakman 2 exemplifies that the experiments performed in mice1 conflict with results in humans carrying the FTO risk allele presenting hyperphagia and increased caloric intake3,4,5,6,7,8,9.

Suggested Citation

  • Julia Fischer & Linda Koch & Christian Emmerling & Jeanette Vierkotten & Thomas Peters & Jens C. Brüning & Ulrich Rüther, 2010. "Fischer et al. reply," Nature, Nature, vol. 464(7289), pages 2-2, April.
    • Handle: RePEc:nat:nature:v:464:y:2010:i:7289:d:10.1038_nature08808
    DOI: 10.1038/nature08808
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