Published December 19, 2018
| Version v1
Journal article
Open
Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria
Creators
-
Day, Felix1
- Karaderi, Tugce2
- Jones, Michelle R.3
-
Meun, Cindy4
- He, Chunyan5
- Drong, Alex2
- Kraft, Peter6
- Lin, Nan5
- Huang, Hongyan6
- Broer, Linda4
- Magi, Reedik7
- Saxena, Richa6
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Laisk, Triin7
- Urbanek, Margrit8
- Hayes, M. Geoffrey8
- Thorleifsson, Gudmar9
- Fernandez-Tajes, Juan2
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Mahajan, Anubha2
- Mullin, Benjamin H.10
- Ehrmann, David11
- 1. University of Cambridge
- 2. University of Oxford
- 3. Cedars-Sinai Medical Center
- 4. Erasmus MC
- 5. University of Kentucky
- 6. Harvard University
- 7. University of Tartu
- 8. Northwestern University
- 9. deCODE genetics/Amgen
- 10. University of Western Australia
- 11. University of Chicago
Description
Polycystic ovary syndrome (PCOS) is a disorder characterized by hyperandrogenism, ovulatory dysfunction and polycystic ovarian morphology. Affected women frequently have metabolic disturbances including insulin resistance and dysregulation of glucose homeostasis. PCOS is diagnosed with two different sets of diagnostic criteria, resulting in a phenotypic spectrum of PCOS cases. The genetic similarities between cases diagnosed based on the two criteria have been largely unknown. Previous studies in Chinese and European subjects have identified 16 loci associated with risk of PCOS. We report a fixed-effect, inverse-weighted-variance meta-analysis from 10,074 PCOS cases and 103,164 controls of European ancestry and characterisation of PCOS related traits. We identified 3 novel loci (near PLGRKT, ZBTB16 and MAPRE1), and provide replication of 11 previously reported loci. Only one locus differed significantly in its association by diagnostic criteria; otherwise the genetic architecture was similar between PCOS diagnosed by self-report and PCOS diagnosed by NIH or non-NIH Rotterdam criteria across common variants at 13 loci. Identified variants were associated with hyperandrogenism, gonadotropin regulation and testosterone levels in affected women. Linkage disequilibrium score regression analysis revealed genetic correlations with obesity, fasting insulin, type 2 diabetes, lipid levels and coronary artery disease, indicating shared genetic architecture between metabolic traits and PCOS. Mendelian randomization analyses suggested variants associated with body mass index, fasting insulin, menopause timing, depression and male-pattern balding play a causal role in PCOS. The data thus demonstrate 3 novel loci associated with PCOS and similar genetic architecture for all diagnostic criteria. The data also provide the first genetic evidence for a male phenotype for PCOS and a causal link to depression, a previously hypothesized comorbid disease. Thus, the genetics provide a comprehensive view of PCOS that encompasses multiple diagnostic criteria, gender, reproductive potential and mental health.
Data availability
Summary statistic GWAS meta-analysis results for the combined dataset excluding 23andMe are available at https://doi.org/10.17863/CAM.27720. The most significant 10,000 SNPs for the meta-analysis including 23andMe are available at https://doi.org/10.17863/CAM.27720.
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Additional details
Identifiers
- DOI
- 10.1371/journal.pgen.1007813
- Other
- oai:uchicago.tind.io:6370
Funding
- Medical Research Council
- MC_U106179472
- Cedars-Sinai Medical Center
- Developmental Funds
- Cedars-Sinai Medical Center
- Developmental Funds
- National Cancer Institute
- P30CA177558
- National Cancer Institute
- UM1CA186107
- European Commission
- European Regional Development Fund
- European Union
- Horizon 2020 research and innovation program
- European Union
- Horizon 2020 research and innovation program
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- R01HD065029
- Ministry of Education and Research
- IUT34-16
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- R01HD057450
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- P50HD044405
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- R01HD057223
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- R01HD085227
- deCODE Genetics (Iceland)
- Raine Medical Research Foundation
- Priming Grant
- Sir Charles Gairdner Osborne Park Health Care Group
- 2015-16/034
- Sir Charles Gairdner Osborne Park Health Care Group
- 2016-17/018
- NIHR BRC
- Wellcome Trust
- Cedars-Sinai Medical Center
- National Institute of Diabetes and Digestive and Kidney Diseases
- P30 DK063491
- National Institute of Diabetes and Digestive and Kidney Diseases
- U01DK094431
- National Institute of Diabetes and Digestive and Kidney Diseases
- U01DK048381
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- U10HD38992
- Ministry of Education and Research
- IUT34-16
- Enterprise Estonia (Estonia)
- EU48695
- 7th Framework Programme, European Commission
- Marie Curie Industry-Academia Partnerships and Pathways
- Wellcome Trust
- 090532
- Wellcome Trust
- 098381
- Wellcome Trust
- 203141
- European Commission
- ENGAGE: HEALTH-F4-2007-201413
- Medical Research Council
- G0802782
- Medical Research Council
- MR/M012638/1
- Li Ka Shing Foundation
- University of Oxford
- John Fell Funds
- NIHR Biomedical Research Centre
- University of Oxford
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- Widenlife
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- R01HD065029
- American Diabetes Association
- 1-10-CT-57
- National Center for Research Resources
- 1UL1 RR025758
- Cedars-Sinai Medical Center