Bryan S Richardson1, Stephanie Ruttinger2, Hilary K Brown3, Timothy R H Regnault4, Barbra de Vrijer5. 1. Department of Obstetrics and Gynecology; Department of Physiology and Pharmacology; Department of Pediatrics; Children's Health Research Institute; Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada. Electronic address: brichar1@uwo.ca. 2. Department of Physiology and Pharmacology; Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada. 3. Department of Obstetrics and Gynecology; Department of Epidemiology & Biostatistics; Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada. 4. Department of Obstetrics and Gynecology; Department of Physiology and Pharmacology; Children's Health Research Institute; Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada. 5. Department of Obstetrics and Gynecology; Children's Health Research Institute; Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada.
Abstract
BACKGROUND: 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. AIMS: To examine linkages between maternal BMI and birth weights, placental weights, and umbilical vein and artery PO2, with implications for signaling mechanisms. STUDY DESIGN: Population-based cohort study. SUBJECTS: 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). OUTCOME MEASURES: Maternal BMI, birth and placental weights, umbilical vein and artery PO2. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. AIMS: To examine linkages between maternal BMI and birth weights, placental weights, and umbilical vein and artery PO2, with implications for signaling mechanisms. STUDY DESIGN: Population-based cohort study. SUBJECTS: 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). OUTCOME MEASURES: Maternal BMI, birth and placental weights, umbilical vein and artery PO2. RESULTS: 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. CONCLUSIONS: 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.
Authors: Bryan S Richardson; Akasham Rajagopaul; Barbra de Vrijer; Genevieve Eastabrook; Timothy R H Regnault Journal: Biol Sex Differ Date: 2022-06-29 Impact factor: 8.811