Genome-wide association study identifies African-ancestry specific variants for metabolic syndrome
The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits...
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| Published in | Molecular genetics and metabolism Vol. 116; no. 4; pp. 305 - 313 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.12.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1096-7192 1096-7206 1096-7206 |
| DOI | 10.1016/j.ymgme.2015.10.008 |
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| Abstract | The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits comprising MetS, the genetic basis and pathophysiological mechanisms underlying the clustering of these traits remain unclear. We conducted GWAS of MetS in 1427 Africans from Ghana and Nigeria followed by replication testing and meta-analysis in another continental African sample from Kenya. Further replication testing was performed in an African American sample from the Atherosclerosis Risk in Communities (ARIC) study. We found two African-ancestry specific variants that were significantly associated with MetS: SNP rs73989312[A] near CA10 that conferred increased risk (P=3.86×10−8, OR=6.80) and SNP rs77244975[C] in CTNNA3 that conferred protection against MetS (P=1.63×10−8, OR=0.15). Given the exclusive expression of CA10 in the brain, our CA10 finding strengthens previously reported link between brain function and MetS. We also identified two variants that are not African specific: rs76822696[A] near RALYL associated with increased MetS risk (P=7.37×10−9, OR=1.59) and rs7964157[T] near KSR2 associated with reduced MetS risk (P=4.52×10−8, Pmeta=7.82×10−9, OR=0.53). The KSR2 locus displayed pleiotropic associations with triglyceride and measures of blood pressure. Rare KSR2 mutations have been reported to be associated with early onset obesity and insulin resistance. Finally, we replicated the LPL and CETP loci previously found to be associated with MetS in Europeans. These findings provide novel insights into the genetics of MetS in Africans and demonstrate the utility of conducting trans-ethnic disease gene mapping studies for testing the cosmopolitan significance of GWAS signals of cardio-metabolic traits.
•African-specific CA10 and CTNNA3 variants are associated with metabolic syndrome.•A common KSR2 variant is associated with a 47% reduced risk for metabolic syndrome.•KSR2 and MBNL1 loci display pleiotropic effects across two or more traits.•A continuous metabolic score identifies loci implicated in metabolic profiles. |
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| AbstractList | The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits comprising MetS, the genetic basis and pathophysiological mechanisms underlying the clustering of these traits remain unclear. We conducted GWAS of MetS in 1427 Africans from Ghana and Nigeria followed by replication testing and meta-analysis in another continental African sample from Kenya. Further replication testing was performed in an African American sample from the Atherosclerosis Risk in Communities (ARIC) study. We found two African-ancestry specific variants that were significantly associated with MetS: SNP rs73989312[A] near CA10 that conferred increased risk (P=3.86 × 10(-8), OR=6.80) and SNP rs77244975[C] in CTNNA3 that conferred protection against MetS (P=1.63 × 10(-8), OR=0.15). Given the exclusive expression of CA10 in the brain, our CA10 finding strengthens previously reported link between brain function and MetS. We also identified two variants that are not African specific: rs76822696[A] near RALYL associated with increased MetS risk (P=7.37 × 10(-9), OR=1.59) and rs7964157[T] near KSR2 associated with reduced MetS risk (P=4.52 × 10(-8), Pmeta=7.82 × 10(-9), OR=0.53). The KSR2 locus displayed pleiotropic associations with triglyceride and measures of blood pressure. Rare KSR2 mutations have been reported to be associated with early onset obesity and insulin resistance. Finally, we replicated the LPL and CETP loci previously found to be associated with MetS in Europeans. These findings provide novel insights into the genetics of MetS in Africans and demonstrate the utility of conducting trans-ethnic disease gene mapping studies for testing the cosmopolitan significance of GWAS signals of cardio-metabolic traits. The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits comprising MetS, the genetic basis and pathophysiological mechanisms underlying the clustering of these traits remain unclear. We conducted GWAS of MetS in 1427 Africans from Ghana and Nigeria followed by replication testing and meta-analysis in another continental African sample from Kenya. Further replication testing was performed in an African American sample from the Atherosclerosis Risk in Communities (ARIC) study. We found two African-ancestry specific variants that were significantly associated with MetS: SNP rs73989312[A] near CA10 that conferred increased risk (P=3.86×10−8, OR=6.80) and SNP rs77244975[C] in CTNNA3 that conferred protection against MetS (P=1.63×10−8, OR=0.15). Given the exclusive expression of CA10 in the brain, our CA10 finding strengthens previously reported link between brain function and MetS. We also identified two variants that are not African specific: rs76822696[A] near RALYL associated with increased MetS risk (P=7.37×10−9, OR=1.59) and rs7964157[T] near KSR2 associated with reduced MetS risk (P=4.52×10−8, Pmeta=7.82×10−9, OR=0.53). The KSR2 locus displayed pleiotropic associations with triglyceride and measures of blood pressure. Rare KSR2 mutations have been reported to be associated with early onset obesity and insulin resistance. Finally, we replicated the LPL and CETP loci previously found to be associated with MetS in Europeans. These findings provide novel insights into the genetics of MetS in Africans and demonstrate the utility of conducting trans-ethnic disease gene mapping studies for testing the cosmopolitan significance of GWAS signals of cardio-metabolic traits. •African-specific CA10 and CTNNA3 variants are associated with metabolic syndrome.•A common KSR2 variant is associated with a 47% reduced risk for metabolic syndrome.•KSR2 and MBNL1 loci display pleiotropic effects across two or more traits.•A continuous metabolic score identifies loci implicated in metabolic profiles. The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits comprising MetS, the genetic basis and pathophysiological mechanisms underlying the clustering of these traits remain unclear. We conducted GWAS of MetS in 1427 Africans from Ghana and Nigeria followed by replication testing and meta-analysis in another continental African sample from Kenya. Further replication testing was performed in an African American sample from the Atherosclerosis Risk in Communities (ARIC) study. We found two African-ancestry specific variants that were significantly associated with MetS: SNP rs73989312[A] near CA10 that conferred increased risk (P=3.86 × 10(-8), OR=6.80) and SNP rs77244975[C] in CTNNA3 that conferred protection against MetS (P=1.63 × 10(-8), OR=0.15). Given the exclusive expression of CA10 in the brain, our CA10 finding strengthens previously reported link between brain function and MetS. We also identified two variants that are not African specific: rs76822696[A] near RALYL associated with increased MetS risk (P=7.37 × 10(-9), OR=1.59) and rs7964157[T] near KSR2 associated with reduced MetS risk (P=4.52 × 10(-8), Pmeta=7.82 × 10(-9), OR=0.53). The KSR2 locus displayed pleiotropic associations with triglyceride and measures of blood pressure. Rare KSR2 mutations have been reported to be associated with early onset obesity and insulin resistance. Finally, we replicated the LPL and CETP loci previously found to be associated with MetS in Europeans. These findings provide novel insights into the genetics of MetS in Africans and demonstrate the utility of conducting trans-ethnic disease gene mapping studies for testing the cosmopolitan significance of GWAS signals of cardio-metabolic traits.The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits comprising MetS, the genetic basis and pathophysiological mechanisms underlying the clustering of these traits remain unclear. We conducted GWAS of MetS in 1427 Africans from Ghana and Nigeria followed by replication testing and meta-analysis in another continental African sample from Kenya. Further replication testing was performed in an African American sample from the Atherosclerosis Risk in Communities (ARIC) study. We found two African-ancestry specific variants that were significantly associated with MetS: SNP rs73989312[A] near CA10 that conferred increased risk (P=3.86 × 10(-8), OR=6.80) and SNP rs77244975[C] in CTNNA3 that conferred protection against MetS (P=1.63 × 10(-8), OR=0.15). Given the exclusive expression of CA10 in the brain, our CA10 finding strengthens previously reported link between brain function and MetS. We also identified two variants that are not African specific: rs76822696[A] near RALYL associated with increased MetS risk (P=7.37 × 10(-9), OR=1.59) and rs7964157[T] near KSR2 associated with reduced MetS risk (P=4.52 × 10(-8), Pmeta=7.82 × 10(-9), OR=0.53). The KSR2 locus displayed pleiotropic associations with triglyceride and measures of blood pressure. Rare KSR2 mutations have been reported to be associated with early onset obesity and insulin resistance. Finally, we replicated the LPL and CETP loci previously found to be associated with MetS in Europeans. These findings provide novel insights into the genetics of MetS in Africans and demonstrate the utility of conducting trans-ethnic disease gene mapping studies for testing the cosmopolitan significance of GWAS signals of cardio-metabolic traits. The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits comprising MetS, the genetic basis and pathophysiological mechanisms underlying the clustering of these traits remain unclear. We conducted GWAS of MetS in 1,427 Africans from Ghana and Nigeria followed by replication testing and meta-analysis in another continental African sample from Kenya. Further replication testing was performed in an African American sample from the Atherosclerosis Risk in Communities (ARIC) study. We found two African-ancestry specific variants that were significantly associated with MetS: SNP rs73989312[A] near CA10 that conferred increased risk ( P =3.86x10 −8 , OR=6.80) and SNP rs77244975[C] in CTNNA3 that conferred protection against MetS (P =1.63x10 −8 , OR=0.15). Given the exclusive expression of CA10 in the brain, our CA10 finding strengthens previously reported link between brain function and MetS. We also identified two variants that are not African specific: rs76822696[A] near RALYL associated with increased MetS risk (P =7.37x10 −9 , OR=1.59) and rs7964157[T] near KSR2 associated with reduced MetS risk ( P =4.52x10 −8 , P meta =7.82x10 −9 , OR=0.53). The KSR2 locus displayed pleiotropic associations with triglyceride and measures of blood pressure. Rare KSR2 mutations have been reported to be associated with early onset obesity and insulin resistance. Finally, we replicated the LPL and CETP loci previously found to be associated with MetS in Europeans. These findings provide novel insights into the genetics of MetS in Africans and demonstrate the utility of conducting trans-ethnic disease gene mapping studies for testing the cosmopolitan significance of GWAS signals of cardio-metabolic traits. |
| Author | Adeyemo, Adebowale Zhou, Jie Adebamowo, Clement Fasanmade, Olufemi Oli, Johnnie Doumatey, Ayo P. Acheampong, Joseph Tekola-Ayele, Fasil Agyenim-Boateng, Kofi Rotimi, Charles N. Bentley, Amy R. Okafor, Godfrey Amoah, Albert Shriner, Daniel Chen, Guanjie Eghan, Benjami A. Johnson, Thomas |
| AuthorAffiliation | e Department of Epidemiology and Public Health, School of Medicine, University of Maryland, Baltimore, MD, USA c University of Nigeria Teaching Hospital, Enugu, Nigeria b University of Lagos, Lagos, Nigeria f University of Ghana Medical School, Department of Medicine, Accra, Ghana d University of Science and Technology, Department of Medicine, Kumasi, Ghana a Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes for Health, Bethesda, MD, USA |
| AuthorAffiliation_xml | – name: c University of Nigeria Teaching Hospital, Enugu, Nigeria – name: a Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes for Health, Bethesda, MD, USA – name: e Department of Epidemiology and Public Health, School of Medicine, University of Maryland, Baltimore, MD, USA – name: f University of Ghana Medical School, Department of Medicine, Accra, Ghana – name: b University of Lagos, Lagos, Nigeria – name: d University of Science and Technology, Department of Medicine, Kumasi, Ghana |
| Author_xml | – sequence: 1 givenname: Fasil surname: Tekola-Ayele fullname: Tekola-Ayele, Fasil email: ayeleft@mail.nih.gov organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA – sequence: 2 givenname: Ayo P. surname: Doumatey fullname: Doumatey, Ayo P. organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA – sequence: 3 givenname: Daniel surname: Shriner fullname: Shriner, Daniel organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA – sequence: 4 givenname: Amy R. surname: Bentley fullname: Bentley, Amy R. organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA – sequence: 5 givenname: Guanjie surname: Chen fullname: Chen, Guanjie organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA – sequence: 6 givenname: Jie surname: Zhou fullname: Zhou, Jie organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA – sequence: 7 givenname: Olufemi surname: Fasanmade fullname: Fasanmade, Olufemi organization: University of Lagos, Lagos, Nigeria – sequence: 8 givenname: Thomas surname: Johnson fullname: Johnson, Thomas organization: University of Lagos, Lagos, Nigeria – sequence: 9 givenname: Johnnie surname: Oli fullname: Oli, Johnnie organization: University of Nigeria Teaching Hospital, Enugu, Nigeria – sequence: 10 givenname: Godfrey surname: Okafor fullname: Okafor, Godfrey organization: University of Nigeria Teaching Hospital, Enugu, Nigeria – sequence: 11 givenname: Benjami A. surname: Eghan fullname: Eghan, Benjami A. organization: University of Science and Technology, Department of Medicine, Kumasi, Ghana – sequence: 12 givenname: Kofi surname: Agyenim-Boateng fullname: Agyenim-Boateng, Kofi organization: University of Science and Technology, Department of Medicine, Kumasi, Ghana – sequence: 13 givenname: Clement surname: Adebamowo fullname: Adebamowo, Clement organization: Department of Epidemiology and Public Health, School of Medicine, University of Maryland, Baltimore, MD, USA – sequence: 14 givenname: Albert surname: Amoah fullname: Amoah, Albert organization: University of Ghana Medical School, Department of Medicine, Accra, Ghana – sequence: 15 givenname: Joseph surname: Acheampong fullname: Acheampong, Joseph organization: University of Science and Technology, Department of Medicine, Kumasi, Ghana – sequence: 16 givenname: Adebowale surname: Adeyemo fullname: Adeyemo, Adebowale organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA – sequence: 17 givenname: Charles N. surname: Rotimi fullname: Rotimi, Charles N. email: rotimic@mail.nih.gov organization: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26507551$$D View this record in MEDLINE/PubMed |
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| Keywords | African ancestry Pleiotropy GWAS MetS NCEP Genome-wide association study T2D Metabolic syndrome cMetS |
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| PublicationDate | 2015-12-01 |
| PublicationDateYYYYMMDD | 2015-12-01 |
| PublicationDate_xml | – month: 12 year: 2015 text: 2015-12-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Molecular genetics and metabolism |
| PublicationTitleAlternate | Mol Genet Metab |
| PublicationYear | 2015 |
| Publisher | Elsevier Inc |
| Publisher_xml | – name: Elsevier Inc |
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| Title | Genome-wide association study identifies African-ancestry specific variants for metabolic syndrome |
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