Richardson Bryan S, Ruttinger Stephanie, Brown Hilary K, Regnault Timothy R H, de Vrijer Barbra
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.
Department of Physiology and Pharmacology; Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada.
Early Hum Dev. 2017 Sep;112:42-47. doi: 10.1016/j.earlhumdev.2017.06.009. Epub 2017 Jul 6.
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 PO 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 PO.
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 PO, consistent with aberrant placental development leading to diffusional impairment of oxygen. Both maternal overweight/obese BMI and LGA resulted in lower artery PO, 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.
已知母体营养不足和营养过剩会影响胎儿生长，改变胎盘发育和营养物质运输，但胎儿氧合是否也会改变尚不清楚。
研究母体体重指数（BMI）与出生体重、胎盘重量以及脐静脉和动脉血氧分压（PO）之间的联系及其对信号传导机制的影响。
基于人群的队列研究。
分析1999年1月1日至2010年12月31日期间所有孕前BMI值的患者分娩存活单胎婴儿的医院数据库信息（N = 29212）。BMI分为体重过轻、正常体重、超重和肥胖，出生体重分为小于胎龄儿（SGA）、适于胎龄儿（AGA）和大于胎龄儿（LGA）。
母体BMI、出生体重和胎盘重量、脐静脉和动脉PO。
婴儿较小的体重过轻母亲和婴儿较大的超重/肥胖母亲胎盘不成比例地大，表明这些妊娠中胎盘生长存在代偿性和/或增强。所有SGA婴儿的脐静脉和动脉PO均较低，这与胎盘发育异常导致氧扩散受损一致。母体超重/肥胖BMI和LGA均导致动脉PO降低，可能是由于这些婴儿体型较大，生长速度加快。
这些发现支持胎儿低氧血症是生长受限的常见决定因素，无论是在体重过轻的母亲中由于营养不足，还是在超重/肥胖的母亲中由于胎盘功能不全。然而，在超重/肥胖母亲和LGA婴儿中，氧气不太可能是胎儿生长的主要促进因素，在这些妊娠中其他营养底物作为营养信号更为重要。
