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Published on: November 1, 2019
Effects of maternal western-style diet on amniotic fluid volume and amnion VEGF profiles in a nonhuman primate model
Cecilia Y Cheung1, Victoria H J Roberts2, Antonio E Frias1,2
1Department of Obstetrics and Gynecology, Oregon Health and Sciences University, Portland, Oregon.
During pregnancy, high fat diet (HFD) induces maternal obesity, insulin resistance, and placental inflammatory responses that compromise placental and fetal development. Whether maternal HFD would adversely affect amniotic fluid volume (AFV) has not been explored. Vascular endothelial growth factor (VEGF) is expressed in the amnion and has been proposed as a regulator of AFV. Our aim was to investigate the effects of HFD on AFV and the associated changes in VEGF and soluble VEGF receptor 1 (sFlt-1) expression profiles in three amnion regions of a nonhuman primate model. Further, we examined the relationships between VEGF expression and HFD-induced changes in maternal metabolic status. Japanese macaques were maintained on control or HFD and amniotic fluid index (AFI) was measured as an ultrasonic estimate of AFV. Amniotic fluid VEGF concentrations were determined by ELISA and amnion VEGF and sFlt-1 mRNA levels by real-time RT-qPCR. HFD increased maternal plasma triglyceride while glucose levels were unchanged. Maternal weight gain was found in diet-sensitive animals whereas amniotic fluid VEGF concentration was reduced in diet-resistant animals. HFD did not alter AFI and there was no correlation between AFI and maternal weight or amniotic fluid VEGF concentrations. VEGF mRNA levels were lowest in secondary placental amnion while sFlt-1 mRNA were lowest in the primary placental amnion. HFD did not affect amnion VEGF or sFlt-1 mRNA expression. These findings suggest that although maternal HFD increased maternal weight in diet-sensitive and reduced amniotic fluid VEGF concentrations in diet-resistant phenotype, AFV as indicated by the AFI, was not significantly affected.
During pregnancy, high fat diet (HFD) induces maternal obesity, insulin resistance, and placental inflammatory responses that compromise placental and fetal development. Whether maternal HFD would adversely affect amniotic fluid volume (AFV) has not been explored. Vascular endothelial growth factor (VEGF) is expressed in the amnion and has been proposed as a regulator of AFV. Our aim was to investigate the effects of HFD on AFV and the associated changes in VEGF and soluble VEGF receptor 1 (sFlt-1) expression profiles in three amnion regions of a nonhuman primate model. Further, we examined the relationships between VEGF expression and HFD-induced changes in maternal metabolic status. Japanese macaques were maintained on control or HFD and amniotic fluid index (AFI) was measured as an ultrasonic estimate of AFV. Amniotic fluid VEGF concentrations were determined by ELISA and amnion VEGF and sFlt-1 mRNA levels by real-time RT-qPCR. HFD increased maternal plasma triglyceride while glucose levels were unchanged. Maternal weight gain was found in diet-sensitive animals whereas amniotic fluid VEGF concentration was reduced in diet-resistant animals. HFD did not alter AFI and there was no correlation between AFI and maternal weight or amniotic fluid VEGF concentrations. VEGF mRNA levels were lowest in secondary placental amnion while sFlt-1 mRNA were lowest in the primary placental amnion. HFD did not affect amnion VEGF or sFlt-1 mRNA expression. These findings suggest that although maternal HFD increased maternal weight in diet-sensitive and reduced amniotic fluid VEGF concentrations in diet-resistant phenotype, AFV as indicated by the AFI, was not significantly affected.
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