Early human development 2017 07 06112() 42-47 pii S0378-3782(17)30173-1
Maternal under- and over-nutrition are known to effect fetal growth with altered placental development and nutrient transport, but whether fetal oxygenation is also altered remains unknown.
To examine linkages between maternal BMI and birth weights, placental weights, and umbilical vein and artery PO2, with implications for signaling mechanisms.
Population-based cohort study.
Analysis of hospital database information on all patients with pre-pregnant BMI values delivering viable, singleton infants between Jan 1, 1999 and Dec 31, 2010 (N=29,212). BMI was categorized into underweight, normal weight, overweight, and obese, with birth weights categorized into small (SGA), appropriate (AGA), and large for gestational age (LGA).
Maternal BMI, birth and placental weights, umbilical vein and artery PO2.
Underweight mothers with smaller infants and overweight/obese mothers with larger infants had disproportionately large placentas, suggesting compensatory and/or enhanced placental growth in these pregnancies. All SGA infants had lower umbilical vein and artery PO2, consistent with aberrant placental development leading to diffusional impairment of oxygen. Both maternal overweight/obese BMI and LGA resulted in lower artery PO2, likely due to increased growth rates with the larger size in these infants.
These findings support fetal hypoxemia as a common determinant of growth restriction, whether in underweight mothers and due to under-nutrition or in overweight/obese mothers and due to placental insufficiency. However, oxygen is unlikely to be the primary promotor for fetal growth in overweight/obese mothers and LGA infants, with other substrates of more importance as nutritional cues in these pregnancies.