ArticleInternational journal of obesity (2005)2015
Human supraphysiological gestational weight gain and fetoplacental vascular dysfunction.
Article in International journal of obesity (2005), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Metabolic abnormalities and obesity's impact on the risk for developing preeclampsia.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Pooled it
- ACE2 downregulation contributes to adverse cardiovascular and reproductive outcomes in female mice on high-fat diet.American journal of physiology. Heart and circulatory physiology · 2026Article
- Placental Pathophysiology and Developmental Programming of Adult Cardiometabolic Risk: A Narrative Review of Pregnancy Exposures.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Maternal Pregestational Body Mass Index and Delivery Outcomes: A Retrospective Study in a Tertiary High-Income Setting.Journal of nutrition and metabolism · 2026Review
- Higher gestational weight gain delays wound healing and reduces expression of long non-coding RNA KLRK1-AS1 in neonatal endothelial progenitor cells.The Journal of physiology · 2023Article
- Pathomechanisms of Prenatally Programmed Adult Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Article
- Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature.Scientific reports · 2018Article
- Effect of maternal high-fat diet on key components of the placental and hepatic endocannabinoid system.American journal of physiology. Endocrinology and metabolism · 2018Article
- Obesity and Preeclampsia: Common Pathophysiological Mechanisms.Frontiers in physiology · 2018Review
- Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy.Journal of diabetes research · 2017Review
- Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Review
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveHuman foetal development and growth in an environment of maternal obesity associates with high risk of cardiovascular disease and adverse neonatal outcome. We studied whether supraphysiological gestational weight gain results in human fetoplacental endothelial dysfunction and altered fetoplacental vascular reactivity.
methodsPrimary cultures of human umbilical vein endothelial cells (HUVECs) and umbilical vein rings were obtained from pregnant women (112 total of patients recruited, 7 patients dropped out) exhibiting prepregnancy normal weight that ended with a physiological (pGWG (n=67), total weight gain 11.5-16 kg, rates of weight gain ≤0.42 kg per week) or supraphysiological (spGWG (n=38), total weight gain >16 kg, rates of weight gain >0.42 kg per week) gestational weight gain (reference values from US Institute of Medicine guidelines). Vascular reactivity to insulin (0.1-1000 nmol l(-1), 5 min) in KCl-preconstricted vein rings was measured using a wire myograph. Protein levels of human equilibrative nucleoside transporter 1 (hENT1), total and Ser(1177)- or Thr(495)-phosphorylated endothelial nitric oxide synthase (eNOS) were detected by western blot or immunofluorescence, and adenosine transport (0-250 μmol l(-1) adenosine, 2 μCi ml(-1) [(3)H]adenosine, 20 s, 25 °C) was measured in the presence or absence of 1 μmol l(-1) nitrobenzylthioinosine (hENT1 inhibitor) or 10 μmol l(-1) chlorpromazine (CPZ, endocytosis inhibitor) in HUVECs.
resultsspGWG associates with reduced NOS activity-dependent dilation of vein rings (P=0.001), lower eNOS expression and higher Thr(495) (P=0.044), but unaltered Ser(1177)eNOS phosphorylation. hENT1-adenosine maximal transport activity was reduced (P=0.041), but the expression was increased (P=0.001) in HUVECs from this group. CPZ increased hENT1-adenosine transport (P=0.040) and hENT1 plasma membrane accumulation only in cells from pGWG.
conclusionspGWG in women with a normal prepregnancy weight causes lower fetoplacental vascular reactivity owing to the downregulation of eNOS activity and adenosine transport in HUVECs. Maternal spGWG is a detrimental condition for human fetoplacental endothelial function and reducing these alterations could result in a better neonate outcome.
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