Janbakhishov, TurabCaglayan, ErkanAcet, FerruhAltunyurt, SabahattinOzer, Erdener2020-12-012020-12-0120200020-72921879-3479https://doi.org/10.1002/ijgo.13346https://hdl.handle.net/11454/61924Objective To determine the role of vascular endothelial growth factor (VEGF) in placental hypoperfusion in obesity. Methods the prospective study enrolled women with a first-trimester singleton pregnancy in Izmir, Turkey, between January and April 2011. Participants were divided into three groups: obese (body mass index [BMI, calculated as weight in kilograms divided by the square of height in meters] >30) with cesarean delivery; normal weight (BMI <30) with vaginal delivery (NVD); and healthy controls (BMI <30) with cesarean delivery. Before delivery, serum C-reactive protein (CRP), and uterine and fetal Doppler measurements were taken. VEGF was evaluated immunohistochemically from the umbilical cord. Results Overall, 109 women completed the study: obesity group (n=13, 11.9%), NVD group (n=50, 45.9%), and control group (n=46, 42.2%). Serum CRP was higher in the obesity group than in the control or NVD groups (P=0.009). VEGF score was highest in the NVD group (9.39 +/- 3.11), and lowest in the obesity group (4.58 +/- 2.78) (P<0.001). VEGF score decreased by 0.81 for each increase in BMI of 1 (P=0.002). Conclusions Maternal obesity was related to decreased VEGF expression. Although not supported by Doppler findings, decreased VEGF expression owing to maternal obesity might trigger endothelial dysfunction and inflammation.en10.1002/ijgo.13346info:eu-repo/semantics/closedAccessFetal vasculatureObesityPlacental vascularityVascular endothelial growth factorVEGFArticle1512231236WOS:0005676975000012-s2.0-8509043951132790905Q1Q1