title: Fetal sex determines the impact of maternal PROGINS progesterone receptor polymorphism on maternal physiology during pregnancy.
abstract: BACKGROUND
  Recent evidence from very rare human diseases suggests that variation in the fetal genome can modify maternal physiology during pregnancy. Here, we tested the hypothesis that fetal sex as a major genetic variant of the fetal genome may affect maternal physiology during pregnancy in genetically susceptible pregnant women.
  
  
  METHODS
  We analyzed the impact of fetal sex on maternal physiology during pregnancy in relationship with the maternal PROGINS progesterone receptor gene polymorphism. Two thousand and eighty-nine (2089) Caucasian women without preexisting diabetes and preexisting hypertension with singleton pregnancies delivering consecutively at the Charité obstetrics department participated in this study.
  
  
  RESULTS
  The maternal PROGINS progesterone receptor polymorphism on its own had no effect on blood pressure, new onset of proteinuria, and total glycated hemoglobin at delivery. However, by considering the offspring's sex, the AA variant of the PROGINS progesterone receptor polymorphism was associated with profound cardiovascular/metabolic effects; mothers carrying both A alleles (AA genotype) delivering a boy had significantly lower systolic blood pressure during the first trimester of pregnancy versus AA mothers delivering girls (107.9+/-10.2 vs. 116.6+/-15.1 mmHg, P = 0.044). Diastolic blood pressure was similarly lower during the first trimester of pregnant AA women delivering boys in comparison with AA women delivering girls (63.4+/-5.7 vs. 68.2+/-10.9 mmHg, P = 0.032). Total glycated hemoglobin at delivery was significantly (P = 0.002) higher in AA mothers delivering boys (6.6+/-0.7%) versus AA mothers delivering girls (5.9+/-0.6%).
  
  
  CONCLUSIONS
  Our study indicates that fetal sex may substantially affect maternal blood pressure as well as glycemic control during pregnancy in genetically susceptible mothers.
authors.affiliation: Center for Cardiovascular Research/Institute of Pharmacology, University of Tübingen, Tübingen, Germany. berthold.hocher@charite.de
authors.forename: Berthold
authors.initials: B
authors.lastname: Hocher
authors.forename: You-Peng
authors.initials: YP
authors.lastname: Chen
authors.forename: Ludwig
authors.initials: L
authors.lastname: Schlemm
authors.forename: Aline
authors.initials: A
authors.lastname: Burdack
authors.forename: Jian
authors.initials: J
authors.lastname: Li
authors.forename: Horst
authors.initials: H
authors.lastname: Halle
authors.forename: Thiemo
authors.initials: T
authors.lastname: Pfab
authors.forename: Philipp
authors.initials: P
authors.lastname: Kalk
authors.forename: Florian
authors.initials: F
authors.lastname: Lang
authors.forename: Michael
authors.initials: M
authors.lastname: Godes
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D005333:Fetus / Q000502:physiology*; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000235:genetics*; D008297:Male; D011110:Polymorphism, Genetic / Q000235:genetics*; D011247:Pregnancy; D011507:Proteinuria / Q000235:genetics; D011980:Receptors, Progesterone / Q000235:genetics*; D012737:Sex Factors
chemical_list: D011980:Receptors, Progesterone