Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria.
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...
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Gespeichert in:
| Autor*in: |
Felix Day [verfasserIn] Tugce Karaderi [verfasserIn] Michelle R Jones [verfasserIn] Cindy Meun [verfasserIn] Chunyan He [verfasserIn] Alex Drong [verfasserIn] Peter Kraft [verfasserIn] Nan Lin [verfasserIn] Hongyan Huang [verfasserIn] Linda Broer [verfasserIn] Reedik Magi [verfasserIn] Richa Saxena [verfasserIn] Triin Laisk [verfasserIn] Margrit Urbanek [verfasserIn] M Geoffrey Hayes [verfasserIn] Gudmar Thorleifsson [verfasserIn] Juan Fernandez-Tajes [verfasserIn] Anubha Mahajan [verfasserIn] Benjamin H Mullin [verfasserIn] Bronwyn G A Stuckey [verfasserIn] Timothy D Spector [verfasserIn] Scott G Wilson [verfasserIn] Mark O Goodarzi [verfasserIn] Lea Davis [verfasserIn] Barbara Obermayer-Pietsch [verfasserIn] André G Uitterlinden [verfasserIn] Verneri Anttila [verfasserIn] Benjamin M Neale [verfasserIn] Marjo-Riitta Jarvelin [verfasserIn] Bart Fauser [verfasserIn] Irina Kowalska [verfasserIn] Jenny A Visser [verfasserIn] Marianne Andersen [verfasserIn] Ken Ong [verfasserIn] Elisabet Stener-Victorin [verfasserIn] David Ehrmann [verfasserIn] Richard S Legro [verfasserIn] Andres Salumets [verfasserIn] Mark I McCarthy [verfasserIn] Laure Morin-Papunen [verfasserIn] Unnur Thorsteinsdottir [verfasserIn] Kari Stefansson [verfasserIn] 23andMe Research Team [verfasserIn] Unnur Styrkarsdottir [verfasserIn] John R B Perry [verfasserIn] Andrea Dunaif [verfasserIn] Joop Laven [verfasserIn] Steve Franks [verfasserIn] Cecilia M Lindgren [verfasserIn] Corrine K Welt [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Übergeordnetes Werk: |
In: PLoS Genetics - Public Library of Science (PLoS), 2005, 14(2018), 12, p e1007813 |
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| Übergeordnetes Werk: |
volume:14 ; year:2018 ; number:12, p e1007813 |
| Links: |
Link aufrufen |
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| DOI / URN: |
10.1371/journal.pgen.1007813 |
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| Katalog-ID: |
DOAJ030540291 |
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| 520 | |a 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. | ||
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10.1371/journal.pgen.1007813 doi (DE-627)DOAJ030540291 (DE-599)DOAJc68abd5b52b94dbab11b2cca436008a6 DE-627 ger DE-627 rakwb eng QH426-470 Felix Day verfasserin aut Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria. 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Genetics Tugce Karaderi verfasserin aut Michelle R Jones verfasserin aut Cindy Meun verfasserin aut Chunyan He verfasserin aut Alex Drong verfasserin aut Peter Kraft verfasserin aut Nan Lin verfasserin aut Hongyan Huang verfasserin aut Linda Broer verfasserin aut Reedik Magi verfasserin aut Richa Saxena verfasserin aut Triin Laisk verfasserin aut Margrit Urbanek verfasserin aut M Geoffrey Hayes verfasserin aut Gudmar Thorleifsson verfasserin aut Juan Fernandez-Tajes verfasserin aut Anubha Mahajan verfasserin aut Benjamin H Mullin verfasserin aut Bronwyn G A Stuckey verfasserin aut Timothy D Spector verfasserin aut Scott G Wilson verfasserin aut Mark O Goodarzi verfasserin aut Lea Davis verfasserin aut Barbara Obermayer-Pietsch verfasserin aut André G Uitterlinden verfasserin aut Verneri Anttila verfasserin aut Benjamin M Neale verfasserin aut Marjo-Riitta Jarvelin verfasserin aut Bart Fauser verfasserin aut Irina Kowalska verfasserin aut Jenny A Visser verfasserin aut Marianne Andersen verfasserin aut Ken Ong verfasserin aut Elisabet Stener-Victorin verfasserin aut David Ehrmann verfasserin aut Richard S Legro verfasserin aut Andres Salumets verfasserin aut Mark I McCarthy verfasserin aut Laure Morin-Papunen verfasserin aut Unnur Thorsteinsdottir verfasserin aut Kari Stefansson verfasserin aut 23andMe Research Team verfasserin aut Unnur Styrkarsdottir verfasserin aut John R B Perry verfasserin aut Andrea Dunaif verfasserin aut Joop Laven verfasserin aut Steve Franks verfasserin aut Cecilia M Lindgren verfasserin aut Corrine K Welt verfasserin aut In PLoS Genetics Public Library of Science (PLoS), 2005 14(2018), 12, p e1007813 (DE-627)485248026 (DE-600)2186725-2 15537404 nnns volume:14 year:2018 number:12, p e1007813 https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/article/c68abd5b52b94dbab11b2cca436008a6 kostenfrei https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/toc/1553-7390 Journal toc kostenfrei https://doaj.org/toc/1553-7404 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2018 12, p e1007813 |
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10.1371/journal.pgen.1007813 doi (DE-627)DOAJ030540291 (DE-599)DOAJc68abd5b52b94dbab11b2cca436008a6 DE-627 ger DE-627 rakwb eng QH426-470 Felix Day verfasserin aut Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria. 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Genetics Tugce Karaderi verfasserin aut Michelle R Jones verfasserin aut Cindy Meun verfasserin aut Chunyan He verfasserin aut Alex Drong verfasserin aut Peter Kraft verfasserin aut Nan Lin verfasserin aut Hongyan Huang verfasserin aut Linda Broer verfasserin aut Reedik Magi verfasserin aut Richa Saxena verfasserin aut Triin Laisk verfasserin aut Margrit Urbanek verfasserin aut M Geoffrey Hayes verfasserin aut Gudmar Thorleifsson verfasserin aut Juan Fernandez-Tajes verfasserin aut Anubha Mahajan verfasserin aut Benjamin H Mullin verfasserin aut Bronwyn G A Stuckey verfasserin aut Timothy D Spector verfasserin aut Scott G Wilson verfasserin aut Mark O Goodarzi verfasserin aut Lea Davis verfasserin aut Barbara Obermayer-Pietsch verfasserin aut André G Uitterlinden verfasserin aut Verneri Anttila verfasserin aut Benjamin M Neale verfasserin aut Marjo-Riitta Jarvelin verfasserin aut Bart Fauser verfasserin aut Irina Kowalska verfasserin aut Jenny A Visser verfasserin aut Marianne Andersen verfasserin aut Ken Ong verfasserin aut Elisabet Stener-Victorin verfasserin aut David Ehrmann verfasserin aut Richard S Legro verfasserin aut Andres Salumets verfasserin aut Mark I McCarthy verfasserin aut Laure Morin-Papunen verfasserin aut Unnur Thorsteinsdottir verfasserin aut Kari Stefansson verfasserin aut 23andMe Research Team verfasserin aut Unnur Styrkarsdottir verfasserin aut John R B Perry verfasserin aut Andrea Dunaif verfasserin aut Joop Laven verfasserin aut Steve Franks verfasserin aut Cecilia M Lindgren verfasserin aut Corrine K Welt verfasserin aut In PLoS Genetics Public Library of Science (PLoS), 2005 14(2018), 12, p e1007813 (DE-627)485248026 (DE-600)2186725-2 15537404 nnns volume:14 year:2018 number:12, p e1007813 https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/article/c68abd5b52b94dbab11b2cca436008a6 kostenfrei https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/toc/1553-7390 Journal toc kostenfrei https://doaj.org/toc/1553-7404 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2018 12, p e1007813 |
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10.1371/journal.pgen.1007813 doi (DE-627)DOAJ030540291 (DE-599)DOAJc68abd5b52b94dbab11b2cca436008a6 DE-627 ger DE-627 rakwb eng QH426-470 Felix Day verfasserin aut Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria. 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Genetics Tugce Karaderi verfasserin aut Michelle R Jones verfasserin aut Cindy Meun verfasserin aut Chunyan He verfasserin aut Alex Drong verfasserin aut Peter Kraft verfasserin aut Nan Lin verfasserin aut Hongyan Huang verfasserin aut Linda Broer verfasserin aut Reedik Magi verfasserin aut Richa Saxena verfasserin aut Triin Laisk verfasserin aut Margrit Urbanek verfasserin aut M Geoffrey Hayes verfasserin aut Gudmar Thorleifsson verfasserin aut Juan Fernandez-Tajes verfasserin aut Anubha Mahajan verfasserin aut Benjamin H Mullin verfasserin aut Bronwyn G A Stuckey verfasserin aut Timothy D Spector verfasserin aut Scott G Wilson verfasserin aut Mark O Goodarzi verfasserin aut Lea Davis verfasserin aut Barbara Obermayer-Pietsch verfasserin aut André G Uitterlinden verfasserin aut Verneri Anttila verfasserin aut Benjamin M Neale verfasserin aut Marjo-Riitta Jarvelin verfasserin aut Bart Fauser verfasserin aut Irina Kowalska verfasserin aut Jenny A Visser verfasserin aut Marianne Andersen verfasserin aut Ken Ong verfasserin aut Elisabet Stener-Victorin verfasserin aut David Ehrmann verfasserin aut Richard S Legro verfasserin aut Andres Salumets verfasserin aut Mark I McCarthy verfasserin aut Laure Morin-Papunen verfasserin aut Unnur Thorsteinsdottir verfasserin aut Kari Stefansson verfasserin aut 23andMe Research Team verfasserin aut Unnur Styrkarsdottir verfasserin aut John R B Perry verfasserin aut Andrea Dunaif verfasserin aut Joop Laven verfasserin aut Steve Franks verfasserin aut Cecilia M Lindgren verfasserin aut Corrine K Welt verfasserin aut In PLoS Genetics Public Library of Science (PLoS), 2005 14(2018), 12, p e1007813 (DE-627)485248026 (DE-600)2186725-2 15537404 nnns volume:14 year:2018 number:12, p e1007813 https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/article/c68abd5b52b94dbab11b2cca436008a6 kostenfrei https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/toc/1553-7390 Journal toc kostenfrei https://doaj.org/toc/1553-7404 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2018 12, p e1007813 |
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10.1371/journal.pgen.1007813 doi (DE-627)DOAJ030540291 (DE-599)DOAJc68abd5b52b94dbab11b2cca436008a6 DE-627 ger DE-627 rakwb eng QH426-470 Felix Day verfasserin aut Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria. 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Genetics Tugce Karaderi verfasserin aut Michelle R Jones verfasserin aut Cindy Meun verfasserin aut Chunyan He verfasserin aut Alex Drong verfasserin aut Peter Kraft verfasserin aut Nan Lin verfasserin aut Hongyan Huang verfasserin aut Linda Broer verfasserin aut Reedik Magi verfasserin aut Richa Saxena verfasserin aut Triin Laisk verfasserin aut Margrit Urbanek verfasserin aut M Geoffrey Hayes verfasserin aut Gudmar Thorleifsson verfasserin aut Juan Fernandez-Tajes verfasserin aut Anubha Mahajan verfasserin aut Benjamin H Mullin verfasserin aut Bronwyn G A Stuckey verfasserin aut Timothy D Spector verfasserin aut Scott G Wilson verfasserin aut Mark O Goodarzi verfasserin aut Lea Davis verfasserin aut Barbara Obermayer-Pietsch verfasserin aut André G Uitterlinden verfasserin aut Verneri Anttila verfasserin aut Benjamin M Neale verfasserin aut Marjo-Riitta Jarvelin verfasserin aut Bart Fauser verfasserin aut Irina Kowalska verfasserin aut Jenny A Visser verfasserin aut Marianne Andersen verfasserin aut Ken Ong verfasserin aut Elisabet Stener-Victorin verfasserin aut David Ehrmann verfasserin aut Richard S Legro verfasserin aut Andres Salumets verfasserin aut Mark I McCarthy verfasserin aut Laure Morin-Papunen verfasserin aut Unnur Thorsteinsdottir verfasserin aut Kari Stefansson verfasserin aut 23andMe Research Team verfasserin aut Unnur Styrkarsdottir verfasserin aut John R B Perry verfasserin aut Andrea Dunaif verfasserin aut Joop Laven verfasserin aut Steve Franks verfasserin aut Cecilia M Lindgren verfasserin aut Corrine K Welt verfasserin aut In PLoS Genetics Public Library of Science (PLoS), 2005 14(2018), 12, p e1007813 (DE-627)485248026 (DE-600)2186725-2 15537404 nnns volume:14 year:2018 number:12, p e1007813 https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/article/c68abd5b52b94dbab11b2cca436008a6 kostenfrei https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/toc/1553-7390 Journal toc kostenfrei https://doaj.org/toc/1553-7404 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2018 12, p e1007813 |
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10.1371/journal.pgen.1007813 doi (DE-627)DOAJ030540291 (DE-599)DOAJc68abd5b52b94dbab11b2cca436008a6 DE-627 ger DE-627 rakwb eng QH426-470 Felix Day verfasserin aut Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria. 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Genetics Tugce Karaderi verfasserin aut Michelle R Jones verfasserin aut Cindy Meun verfasserin aut Chunyan He verfasserin aut Alex Drong verfasserin aut Peter Kraft verfasserin aut Nan Lin verfasserin aut Hongyan Huang verfasserin aut Linda Broer verfasserin aut Reedik Magi verfasserin aut Richa Saxena verfasserin aut Triin Laisk verfasserin aut Margrit Urbanek verfasserin aut M Geoffrey Hayes verfasserin aut Gudmar Thorleifsson verfasserin aut Juan Fernandez-Tajes verfasserin aut Anubha Mahajan verfasserin aut Benjamin H Mullin verfasserin aut Bronwyn G A Stuckey verfasserin aut Timothy D Spector verfasserin aut Scott G Wilson verfasserin aut Mark O Goodarzi verfasserin aut Lea Davis verfasserin aut Barbara Obermayer-Pietsch verfasserin aut André G Uitterlinden verfasserin aut Verneri Anttila verfasserin aut Benjamin M Neale verfasserin aut Marjo-Riitta Jarvelin verfasserin aut Bart Fauser verfasserin aut Irina Kowalska verfasserin aut Jenny A Visser verfasserin aut Marianne Andersen verfasserin aut Ken Ong verfasserin aut Elisabet Stener-Victorin verfasserin aut David Ehrmann verfasserin aut Richard S Legro verfasserin aut Andres Salumets verfasserin aut Mark I McCarthy verfasserin aut Laure Morin-Papunen verfasserin aut Unnur Thorsteinsdottir verfasserin aut Kari Stefansson verfasserin aut 23andMe Research Team verfasserin aut Unnur Styrkarsdottir verfasserin aut John R B Perry verfasserin aut Andrea Dunaif verfasserin aut Joop Laven verfasserin aut Steve Franks verfasserin aut Cecilia M Lindgren verfasserin aut Corrine K Welt verfasserin aut In PLoS Genetics Public Library of Science (PLoS), 2005 14(2018), 12, p e1007813 (DE-627)485248026 (DE-600)2186725-2 15537404 nnns volume:14 year:2018 number:12, p e1007813 https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/article/c68abd5b52b94dbab11b2cca436008a6 kostenfrei https://doi.org/10.1371/journal.pgen.1007813 kostenfrei https://doaj.org/toc/1553-7390 Journal toc kostenfrei https://doaj.org/toc/1553-7404 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2018 12, p e1007813 |
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Felix Day @@aut@@ Tugce Karaderi @@aut@@ Michelle R Jones @@aut@@ Cindy Meun @@aut@@ Chunyan He @@aut@@ Alex Drong @@aut@@ Peter Kraft @@aut@@ Nan Lin @@aut@@ Hongyan Huang @@aut@@ Linda Broer @@aut@@ Reedik Magi @@aut@@ Richa Saxena @@aut@@ Triin Laisk @@aut@@ Margrit Urbanek @@aut@@ M Geoffrey Hayes @@aut@@ Gudmar Thorleifsson @@aut@@ Juan Fernandez-Tajes @@aut@@ Anubha Mahajan @@aut@@ Benjamin H Mullin @@aut@@ Bronwyn G A Stuckey @@aut@@ Timothy D Spector @@aut@@ Scott G Wilson @@aut@@ Mark O Goodarzi @@aut@@ Lea Davis @@aut@@ Barbara Obermayer-Pietsch @@aut@@ André G Uitterlinden @@aut@@ Verneri Anttila @@aut@@ Benjamin M Neale @@aut@@ Marjo-Riitta Jarvelin @@aut@@ Bart Fauser @@aut@@ Irina Kowalska @@aut@@ Jenny A Visser @@aut@@ Marianne Andersen @@aut@@ Ken Ong @@aut@@ Elisabet Stener-Victorin @@aut@@ David Ehrmann @@aut@@ Richard S Legro @@aut@@ Andres Salumets @@aut@@ Mark I McCarthy @@aut@@ Laure Morin-Papunen @@aut@@ Unnur Thorsteinsdottir @@aut@@ Kari Stefansson @@aut@@ 23andMe Research Team @@aut@@ Unnur Styrkarsdottir @@aut@@ John R B Perry @@aut@@ Andrea Dunaif @@aut@@ Joop Laven @@aut@@ Steve Franks @@aut@@ Cecilia M Lindgren @@aut@@ Corrine K Welt @@aut@@ |
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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. 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large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria |
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Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria. |
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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. |
| abstractGer |
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. |
| abstract_unstemmed |
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. |
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Large-scale genome-wide meta-analysis of polycystic ovary syndrome suggests shared genetic architecture for different diagnosis criteria. |
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Tugce Karaderi Michelle R Jones Cindy Meun Chunyan He Alex Drong Peter Kraft Nan Lin Hongyan Huang Linda Broer Reedik Magi Richa Saxena Triin Laisk Margrit Urbanek M Geoffrey Hayes Gudmar Thorleifsson Juan Fernandez-Tajes Anubha Mahajan Benjamin H Mullin Bronwyn G A Stuckey Timothy D Spector Scott G Wilson Mark O Goodarzi Lea Davis Barbara Obermayer-Pietsch André G Uitterlinden Verneri Anttila Benjamin M Neale Marjo-Riitta Jarvelin Bart Fauser Irina Kowalska Jenny A Visser Marianne Andersen Ken Ong Elisabet Stener-Victorin David Ehrmann Richard S Legro Andres Salumets Mark I McCarthy Laure Morin-Papunen Unnur Thorsteinsdottir Kari Stefansson 23andMe Research Team Unnur Styrkarsdottir John R B Perry Andrea Dunaif Joop Laven Steve Franks Cecilia M Lindgren Corrine K Welt |
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