Fischer et al. reply

Julia Fischer, Linda Koch, Christian Emmerling, Jeanette Vierkotten, Thomas Peters, Jens C. Brüning and Ulrich Rüther
Additional contact information
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
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
Thomas Peters: * Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany. ruether@uni-duesseldorf.de
Jens C. Brüning: University of Cologne
Ulrich Rüther: * Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany. ruether@uni-duesseldorf.de

Nature, 2010, vol. 464, issue 7289, E2-E2

Abstract: 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.

Date: 2010
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DOI: 10.1038/nature08808

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