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A rare human variant that disrupts GPR10 signalling causes weight gain in mice

Author

Listed:
  • Fleur Talbot

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Claire H. Feetham

    (Faculty of Biology, Medicine and Health, University of Manchester)

  • Jacek Mokrosiński

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Katherine Lawler

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Julia M. Keogh

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Elana Henning

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Edson Mendes de Oliveira

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Vikram Ayinampudi

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Sadia Saeed

    (Digestion and Reproduction, Imperial College London
    European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille University Hospital
    Université de Lille)

  • Amélie Bonnefond

    (Digestion and Reproduction, Imperial College London
    European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille University Hospital
    Université de Lille)

  • Mohammed Arslan

    (Forman Christian College)

  • Giles S. H. Yeo

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital
    Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

  • Philippe Froguel

    (Digestion and Reproduction, Imperial College London
    European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille University Hospital
    Université de Lille)

  • David A. Bechtold

    (Faculty of Biology, Medicine and Health, University of Manchester)

  • Antony Adamson

    (Medicine and Health, University of Manchester)

  • Neil Humphreys

    (Medicine and Health, University of Manchester)

  • Inês Barroso

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital
    University of Cambridge
    University of Exeter Medical School)

  • Simon M. Luckman

    (Faculty of Biology, Medicine and Health, University of Manchester)

  • I. Sadaf Farooqi

    (Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital)

Abstract

Disruption of brain-expressed G protein-coupled receptor-10 (GPR10) causes obesity in animals. Here, we identify multiple rare variants in GPR10 in people with severe obesity and in normal weight controls. These variants impair ligand binding and G protein-dependent signalling in cells. Transgenic mice harbouring a loss of function GPR10 variant found in an individual with obesity, gain excessive weight due to decreased energy expenditure rather than increased food intake. This evidence supports a role for GPR10 in human energy homeostasis. Therapeutic targeting of GPR10 may represent an effective weight-loss strategy.

Suggested Citation

  • Fleur Talbot & Claire H. Feetham & Jacek Mokrosiński & Katherine Lawler & Julia M. Keogh & Elana Henning & Edson Mendes de Oliveira & Vikram Ayinampudi & Sadia Saeed & Amélie Bonnefond & Mohammed Arsl, 2023. "A rare human variant that disrupts GPR10 signalling causes weight gain in mice," Nature Communications, Nature, vol. 14(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-36966-3
    DOI: 10.1038/s41467-023-36966-3
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    References listed on IDEAS

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    1. Shuji Hinuma & Yugo Habata & Ryo Fujii & Yuji Kawamata & Masaki Hosoya & Shoji Fukusumi & Chieko Kitada & Yoshinori Masuo & Tsuneo Asano & Hirokazu Matsumoto & Masahiro Sekiguchi & Tsutomu Kurokawa & , 1998. "A prolactin-releasing peptide in the brain," Nature, Nature, vol. 393(6682), pages 272-276, May.
    2. Shuji Hinuma & Yugo Habata & Ryo Fujii & Yuji Kawamata & Masaki Hosoya & Shoji Fukusumi & Chieko Kitada & Yoshinori Masuo & Tsuneo Asano & Hirokazu Matsumoto & Masahiro Sekiguchi & Tsutomu Kurokawa & , 1998. "A prolactin-releasing peptide in the brain," Nature, Nature, vol. 394(6690), pages 302-302, July.
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