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Maternal and fetal genetic contribution to gestational weight gain.
Int. J. Obes. 42, 755-784 (2018)
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 â '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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Scopus SNIP
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Times Cited
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5.151
1.545
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17
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Planarian Schmidtea-mediterranea; Stem-cells; Rna-seq; Gene-expression; Regeneration; Pluripotency; Trajectories; Organism; Tissues; System
Language
english
Publication Year
2018
Prepublished in Year
2017
HGF-reported in Year
2017
ISSN (print) / ISBN
0307-0565
e-ISSN
1476-5497
Journal
International Journal of Obesity
Quellenangaben
Volume: 42,
Issue: 4,
Pages: 755-784
Publisher
Nature Publishing Group
Publishing Place
1200 New York Ave, Nw, Washington, Dc 20005 Usa
Reviewing status
Peer reviewed
Institute(s)
Institute of Epidemiology (EPI)
POF-Topic(s)
30202 - Environmental Health
30503 - Chronic Diseases of the Lung and Allergies
30503 - Chronic Diseases of the Lung and Allergies
Research field(s)
Genetics and Epidemiology
PSP Element(s)
G-504000-008
G-504091-002
G-504000-009
G-503900-001
G-504091-002
G-504000-009
G-503900-001
WOS ID
WOS:000432681200024
Scopus ID
85047253737
PubMed ID
28990592
Erfassungsdatum
2017-10-12