IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v11y2020i1d10.1038_s41467-020-19595-y.html
   My bibliography  Save this article

Autozygosity influences cardiometabolic disease-associated traits in the AWI-Gen sub-Saharan African study

Author

Listed:
  • Francisco C. Ceballos

    (Sydney Brenner Institute for Molecular Bioscience, Faculty of Health Sciences, University of the Witwatersrand)

  • Scott Hazelhurst

    (Sydney Brenner Institute for Molecular Bioscience, Faculty of Health Sciences, University of the Witwatersrand
    University of the Witwatersrand)

  • David W. Clark

    (University of Edinburgh)

  • Godfred Agongo

    (Sydney Brenner Institute for Molecular Bioscience, Faculty of Health Sciences, University of the Witwatersrand
    Navrongo Health Research Centre)

  • Gershim Asiki

    (African Population and Health Research Center)

  • Palwende R. Boua

    (Sydney Brenner Institute for Molecular Bioscience, Faculty of Health Sciences, University of the Witwatersrand
    Faculty of Health Sciences University of the Witwatersrand, Division of Human Genetics, National Health Laboratory Service and School of Pathology
    Clinical Research Unit of Nanoro, Institut de Recherche en Sciences de la Santé)

  • F. Xavier Gómez-Olivé

    (MRC/Wits Rural Public Health and Health Transitions Research Unit (Agincourt), School of Public Health, Faculty of Health Sciences, University of the Witwatersrand)

  • Felistas Mashinya

    (Department of Pathology and Medical Science, School of Health Care Sciences, Faculty of Health Sciences, University of Limpopo)

  • Shane Norris

    (Sydney Brenner Institute for Molecular Bioscience, Faculty of Health Sciences, University of the Witwatersrand
    Faculty of Health Sciences University of the Witwatersrand, Division of Human Genetics, National Health Laboratory Service and School of Pathology)

  • James F. Wilson

    (University of Edinburgh
    Medical Research Council Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital)

  • Michèle Ramsay

    (Sydney Brenner Institute for Molecular Bioscience, Faculty of Health Sciences, University of the Witwatersrand
    Faculty of Health Sciences University of the Witwatersrand, Division of Human Genetics, National Health Laboratory Service and School of Pathology)

Abstract

The analysis of the effects of autozygosity, measured as the change of the mean value of a trait among offspring of genetic relatives, reveals the existence of directional dominance or overdominance. In this study we detect evidence of the effect of autozygosity in 4 out of 13 cardiometabolic disease-associated traits using data from more than 10,000 sub-Saharan African individuals recruited from Ghana, Burkina Faso, Kenya and South Africa. The effect of autozygosity on these phenotypes is found to be sex-related, with inbreeding having a significant decreasing effect in men but a significant increasing effect in women for several traits (body mass index, subcutaneous adipose tissue, low-density lipoproteins and total cholesterol levels). Overall, the effect of inbreeding depression is more intense in men. Differential effects of inbreeding depression are also observed between study sites with different night-light intensity used as proxy for urban development. These results suggest a directional dominant genetic component mediated by environmental interactions and sex-specific differences in genetic architecture for these traits in the Africa Wits-INDEPTH partnership for Genomic Studies (AWI-Gen) cohort.

Suggested Citation

  • Francisco C. Ceballos & Scott Hazelhurst & David W. Clark & Godfred Agongo & Gershim Asiki & Palwende R. Boua & F. Xavier Gómez-Olivé & Felistas Mashinya & Shane Norris & James F. Wilson & Michèle Ram, 2020. "Autozygosity influences cardiometabolic disease-associated traits in the AWI-Gen sub-Saharan African study," Nature Communications, Nature, vol. 11(1), pages 1-8, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19595-y
    DOI: 10.1038/s41467-020-19595-y
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-020-19595-y
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-020-19595-y?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19595-y. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.