• A Corrigendum to this article was published on 01 October 2007

This article has been updated

Abstract

We identified a set of SNPs in the first intron of the FTO (fat mass and obesity associated) gene on chromosome 16q12.2 that is consistently strongly associated with early-onset and severe obesity in both adults and children of European ancestry with an experiment-wise P value of 1.67 × 10−26 in 2,900 affected individuals and 5,100 controls. The at-risk haplotype yields a proportion of attributable risk of 22% for common obesity. We conclude that FTO contributes to human obesity and hence may be a target for subsequent functional analyses.

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Change history

  • 26 September 2007

    In the version of this article initially published, the authors failed to acknowledge that recruitment of obese cases was supported by both Assistance-Publique Hôpitaux de Paris and Centre National de la Recherche Scientifique. This error has been corrected in the PDF version of the article.

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Acknowledgements

The authors thank M. Deweirder and F. Allegaert for DNA preparation and D.-A. Tregouet for discussions on statistics. This study was supported by the ANR Diabomics grant from the French National Agency for Research. Work on the German replication data set was supported by grants from the DFG (KFO 152: “Atherobesity”, project KO 3512/1–1 (TP 1) to A.K. and 1264/10–1 (TP5) to W.K.) and from the EC (“PIONEER” integrated project grant to W.K.). The Leipzig Schoolchildren project was supported by unrestricted grants from Pfizer Pharma and Novo Nordisk (W.K.).

Author information

Affiliations

  1. CNRS 8090-Institute of Biology, Pasteur Institute, Lille, France.

    • Christian Dina
    • , David Meyre
    • , Sophie Gallina
    • , Emmanuelle Durand
    • , Vincent Vatin
    • , Cecile Lecoeur
    • , Jérome Delplanque
    • , Emmanuel Vaillant
    • , Stéphane Cauchi
    • , Jean-Claude Chèvre
    •  & Philippe Froguel
  2. University Hospital for Children and Adolescents, University of Leipzig, Leipzig, Germany.

    • Antje Körner
    •  & Wieland Kiess
  3. Department of Molecular and Clinical Medicine, Institute of Medicine, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.

    • Peter Jacobson
    •  & Lena M S Carlsson
  4. INSERM U859, Université de Lille 2, Lille, France.

    • François Pattou
  5. Diabétologie et Métabolisme, Centre Hospitalier Universitaire Vaudois (CHUV) BH19, Lausanne, Switzerland.

    • Juan Ruiz
  6. Paediatric Endocrine Unit, Jeanne de Flandre Hospital, Lille, France.

    • Jacques Weill
  7. INSERM U690, Robert Debre Hospital, Paris, France.

    • Claire Levy-Marchal
  8. Klinik Lindberg, Winterthur, Switzerland.

    • Fritz Horber
    •  & Natascha Potoczna
  9. INSERM, U557, Bobigny, France; Institut Scientifique de Recherche Agronomique (INRA), U1125, Bobigny, France; Conservatoire National des Arts et Métiers (CNAM), EA3200, Paris, France; Paris 13 University, Bobigny, France; and Centre de Recherche en Nutrition Humaine (CRNH) Ile de France, Bobigny, France

    • Serge Hercberg
  10. Department of Pediatric Endocrinology and INSERM U561, Saint Vincent de Paul Hospital, René Descartes University, Paris, France.

    • Catherine Le Stunff
    •  & Pierre Bougnères
  11. Department of Internal Medicine III and Interdisciplinary Centre for Clinical Research, University of Leipzig, Leipzig, Germany.

    • Peter Kovacs
  12. Department of Diabetology, Bichat Claude Bernard Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.

    • Michel Marre
  13. INSERM U780-IFR69, Villejuif, France.

    • Beverley Balkau
  14. Université Paris-Sud, Villejuif, France.

    • Beverley Balkau
  15. Genomic Medicine, Hammersmith Hospital, Imperial College London, London, UK.

    • Philippe Froguel

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Contributions

Contributions of each author are detailed in the Supplementary Note online.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to Christian Dina.

Supplementary information

PDF files

  1. 1.

    Supplementary Fig. 1

    LD in the FTO gene.

  2. 2.

    Supplementary Fig. 2

    FTO gene expression in human tissues.

  3. 3.

    Supplementary Table 1

    Assessment of putative functionality of SNPs.

  4. 4.

    Supplementary Table 2

    Genotype distribution and association tests under the general and additive models.

  5. 5.

    Supplementary Table 3

    Genotype counts, Hardy Weinberg tests and failed genotype rate.

  6. 6.

    Supplementary Table 4

    Effect size estimation and quantitative trait associations.

  7. 7.

    Supplementary Table 5

    Description of study populations.

  8. 8.

    Supplementary Table 6

    LD with potentially associated SNPs.

  9. 9.

    Supplementary Methods

  10. 10.

    Supplementary Notes

About this article

Publication history

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Published

DOI

https://doi.org/10.1038/ng2048

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