Liliana Aguayo1,2,3, Weiqin Li4, Brian T Joyce5, Junhong Leng4, Yinan Zheng5, Stephanie Shiau6, Huikun Liu4, Leishen Wang4, Ru Gao7, Andrea Baccarelli8, Gang Hu7, Lifang Hou5. 1. Department of Preventive Medicine, Feinberg School of Medicine; Northwestern University, Chicago, IL, USA. 2. Mary Ann and J. Milburn Smith Child Health Research, Outreach, and Advocacy Center, Stanley Manne Children's Research Institute, Ann and Robert H. Lurie Children's Hospital, Chicago, IL, USA. 3. Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA. 4. Tianjin Women's and Children's Health Center, Tianjin, China. 5. Department of Preventive Medicine, Center for Global Oncology, Institute for Global Health, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. 6. Department of Biostatistics and Epidemiology, Rutgers School of Public Health, Piscataway, NJ, USA. 7. Chronic Disease Epidemiology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, USA. 8. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA.
Abstract
Background: Gestational diabetes mellitus (GDM) is a major macrosomia risk factor. Variations in the catechol-O-methyltransferase (COMT; rs4680) genotypes are associated with heightened susceptibility to environmental exposures and nutritional conditions. However, macrosomia risks associated with COMT genetics, epigenetics, and the interaction between genetic and epigenetics among children with and without exposure to GDM are unknown. Methods: Data from women/children pairs (n = 1087) who participated in the Tianjin Gestational Diabetes Birth Cohort were used to examine the odds of being born with macrosomia associated with COMT-genotypes, 55 CpG sites located on the COMT gene, and genetic and epigenetic interactions. Odds of macrosomia associated with COMT genetic, epigenetic, genetic and epigenetic interactions, and moderations with GDM were tested using adjusted logistic regression models. Results: Overall, 16.1% (n = 175) of children were born with macrosomia. Models showed that children with at least one copy of the minor allele (A) had higher odds of macrosomia (odds ratio, 1.82; 95% confidence interval 1.25-2.64) compared with children with the GG-genotype. After false discovery rate corrections, none of the 55 CpG sites located on the COMT gene was associated with odds of macrosomia. The genetic and epigenetic associations were not modified by exposure to GDM. Conclusion: Findings suggest carriers of the COMT GG-genotype had lower odds of macrosomia, and this association was not modified by epigenetics or exposure to GDM.
Background: Gestational diabetes mellitus (GDM) is a major macrosomia risk factor. Variations in the catechol-O-methyltransferase (COMT; rs4680) genotypes are associated with heightened susceptibility to environmental exposures and nutritional conditions. However, macrosomia risks associated with COMT genetics, epigenetics, and the interaction between genetic and epigenetics among children with and without exposure to GDM are unknown. Methods: Data from women/children pairs (n = 1087) who participated in the Tianjin Gestational Diabetes Birth Cohort were used to examine the odds of being born with macrosomia associated with COMT-genotypes, 55 CpG sites located on the COMT gene, and genetic and epigenetic interactions. Odds of macrosomia associated with COMT genetic, epigenetic, genetic and epigenetic interactions, and moderations with GDM were tested using adjusted logistic regression models. Results: Overall, 16.1% (n = 175) of children were born with macrosomia. Models showed that children with at least one copy of the minor allele (A) had higher odds of macrosomia (odds ratio, 1.82; 95% confidence interval 1.25-2.64) compared with children with the GG-genotype. After false discovery rate corrections, none of the 55 CpG sites located on the COMT gene was associated with odds of macrosomia. The genetic and epigenetic associations were not modified by exposure to GDM. Conclusion: Findings suggest carriers of the COMT GG-genotype had lower odds of macrosomia, and this association was not modified by epigenetics or exposure to GDM.
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