Inactivation of the Fto gene protects from obesity
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
Linda Koch: Department of Mouse Genetics and Metabolism, Institute for Genetics and Second Department of Internal Medicine,
Christian Emmerling: Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany
Jeanette Vierkotten: Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany
Thomas Peters: Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany
Jens C. Brüning: Department of Mouse Genetics and Metabolism, Institute for Genetics and Second Department of Internal Medicine,
Ulrich Rüther: Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany
Nature, 2009, vol. 458, issue 7240, 894-898
Abstract:
Protection from obesity Variations in the human FTO gene have been linked to obesity-related traits in several genome-wide association studies. A functional correlation is now reported between Fto, the equivalent gene in the mouse, and obesity. In Fto-deficient mice there is postnatal growth retardation and a lean phenotype with high energy expenditure and reduced fat accumulation. This suggests that Fto/FTO is involved in homeostasis via the control of energy expenditure.
Date: 2009
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:458:y:2009:i:7240:d:10.1038_nature07848
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DOI: 10.1038/nature07848
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