Article open access publication

Maternal and fetal genetic contribution to gestational weight gain

International Journal of Obesity, Springer Nature, ISSN 1476-5497

Volume 42, 4, 2018

DOI:10.1038/ijo.2017.248, Dimensions: pub.1092131667, PMC: PMC5784805, PMID: 28990592,

Authors

Warrington, N M (1) (2)
Myhre, R (5)
Wang, C A (2)
Das, S (8)
Murcia, M (9) (10)
Espinosa, A (10) (12) (13) (14)
Thiering, E (15) (16)
Atalay, M (17)
Ntalla, I (19)
Freathy, R (3) (7)
Tiesler, C M T (15) (16)
Allard, C (22)
Crawford, A (3) (23)
Ring, S M (3)
Melbye, M (4) (20) (24)
Magnus, P (5)
Skotte, L (4)
Hansen, T (20)
Marsh, J (2)
Guxens, M (10) (12) (13) (25)
Grallert, H (16) (26) (27) (28)
Lindi, V (17)
Pahkala, K (18) (31)
Standl, M (16)
Marina, L Santa (10) (35)
Kogevinas, M (10) (12) (13) (14)
Heinrich, J (16) (38)
Lakka, T (17) (39) (40)
Zeggini, E (32)
Raitakari, O T (18) (36)
Chatzi, L (30) (41) (42)
Inskip, H M (11) (43)
Bustamante, M (10) (12) (13) (44)
Hivert, M-F (45) (46)
Jarvelin, M-R (8) (21) (47)
Sørensen, T I A (20) (48)
Jacobsson, B (49) (50)
Geller, F (4)
Evans, D M * (1) (3)
Lawlor, D A * (3)

* Corresponding author

Affiliations

Organisations

  1. (1) University of Queensland, grid.1003.2
  2. (2) University of Western Australia, grid.1012.2
  3. (3) University of Bristol, grid.5337.2
  4. (4) State Serum Institute, grid.6203.7
  5. (5) Norwegian Institute of Public Health, grid.418193.6
  6. (6) Erasmus University Medical Center, grid.5645.2
  7. (7) Institute of Biomedical and Clinical Science, University of Exeter Medical School, University of Exeter, Royal Devon and Exeter Hospital, Exeter, UK
  8. (8) Imperial College London, grid.7445.2
  9. (9) Epidemiology and Environmental Health Joint Research Unit, FISABIO–Universitat Jaume I–Universitat de València, Valencia, Spain
  10. (10) Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), Spain
  11. (11) University of Southampton, grid.5491.9
  12. (12) ISGlobal, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain
  13. (13) Pompeu Fabra University, grid.5612.0
  14. (14) Hospital Del Mar, grid.411142.3
  15. (15) Klinikum der Universität München, grid.411095.8
  16. (16) Helmholtz Zentrum München, grid.4567.0
  17. (17) University of Eastern Finland, grid.9668.1
  18. (18) University of Turku, grid.1374.1
  19. (19) Queen Mary University of London, grid.4868.2
  20. (20) University of Copenhagen, grid.5254.6, KU
  21. (21) University of Oulu, grid.10858.34
  22. (22) Centre Hospitalier Universitaire de Sherbrooke, grid.411172.0
  23. (23) University of Edinburgh, grid.4305.2
  24. (24) Stanford University, grid.168010.e
  25. (25) Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre–Sophia Children's Hospital, Rotterdam, The Netherlands
  26. (26) Friedrich Loeffler Institute, grid.417834.d
  27. (27) German Center for Diabetes Research, grid.452622.5
  28. (28) Technical University of Munich, grid.6936.a
  29. (29) Northwestern University, grid.16753.36
  30. (30) University of Crete, grid.8127.c
  31. (31) Department of Health and Physical Activity, Paavo Nurmi Centre, Sports and Exercise Medicine Unit, Turku, Finland
  32. (32) Wellcome Sanger Institute, grid.10306.34
  33. (33) Université de Sherbrooke, grid.86715.3d
  34. (34) Basque Government, grid.431260.2
  35. (35) Biodonostia, grid.432380.e
  36. (36) Turku University Hospital, grid.410552.7
  37. (37) Harokopio University, grid.15823.3d
  38. (38) Institute and Outpatient Clinic for Occupational, Social and Environmental Medicine, Inner City Clinic, University Hospital Munich, Ludwig Maximilian University of Munich, Munich, Germany
  39. (39) Department of Clinical Physiology and Nuclear Medicine, Kuopio University Hospital, School of Medicine, University of Eastern Finland, Kuopio, Finland
  40. (40) Kuopion Liikuntalääketieteen Tutkimuslaitos, grid.419013.e
  41. (41) Maastricht University, grid.5012.6
  42. (42) University of Southern California, grid.42505.36
  43. (43) University Hospital Southampton NHS Foundation Trust, grid.430506.4
  44. (44) Centre for Genomic Regulation, grid.11478.3b
  45. (45) Harvard University, grid.38142.3c
  46. (46) Massachusetts General Hospital, grid.32224.35
  47. (47) Oulu University Hospital, grid.412326.0
  48. (48) Bispebjerg Hospital, grid.411702.1, Capital Region
  49. (49) Department of Genetics and Bioinformatics, Domain of Health Data and Digitalization, Institute of Public Health, Oslo, Norway
  50. (50) University of Gothenburg, grid.8761.8

Description

BACKGROUND: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG. PARTICIPANTS AND METHODS: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight). RESULTS: Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG. CONCLUSIONS: We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.

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Times Cited: 12

Field Citation Ratio (FCR): 11.69

Relative Citation ratio (RCR): 1.69

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