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Maternal insulin-like growth factor binding protein-1, body mass index, and fetal growth

R P Holmes1, J M Holly, P W Soothill

  • 1Fetal Medicine Research Unit, University of Bristol, St Michael's Hospital, Southwell Street, Bristol BS2 8EG, UK.

Archives of Disease in Childhood. Fetal and Neonatal Edition
|February 24, 2000
PubMed

Insights

Maternal insulin-like growth factor binding protein-1 (IGFBP-1) may impact fetal growth. Elevated IGFBP-1 in fetal growth restriction (FGR) might worsen placental function and constrain fetal development.

Area of Science:

  • Reproductive Biology
  • Endocrinology
  • Perinatology

Background:

  • The maternal insulin-like growth factor (IGF) system plays a crucial role in fetal development.
  • Dysregulation of the IGF system has been implicated in abnormal fetal growth.
  • Insulin-like growth factor binding protein-1 (IGFBP-1) is a key regulator within this system.

Purpose of the Study:

  • To investigate the hypothesis that maternal IGFBP-1 influences fetal growth.
  • To compare IGFBP-1 levels in neonates with fetal growth restriction (FGR) versus small for gestational age (SGA) infants and controls.
  • To explore the relationship between maternal IGFBP-1, placental function, and fetal growth parameters.

Main Methods:

  • Prospective observational study involving neonates with birthweights below the 5th centile.
  • Classification of neonates into FGR (placental dysfunction) and SGA (normal placental function) groups.
  • Measurement of maternal serum IGFBP-1 using radioimmunoassay in 25 FGR, 27 SGA, and 89 control infants.
  • Assessment of umbilical artery Doppler pulsatility index (PI), growth velocity, and amniotic fluid.

Main Results:

  • Maternal IGFBP-1 levels were significantly increased in the FGR group (109 ng/ml) compared to SGA (69 ng/ml) and control (57 ng/ml) groups, even after adjusting for maternal BMI.
  • Elevated IGFBP-1 in FGR correlated with increased umbilical artery PI, indicating impaired placental perfusion.
  • No significant correlation between IGFBP-1 and birthweight was observed in control infants after adjusting for BMI.

Conclusions:

  • Maternal IGFBP-1 is unlikely to be involved in normal placental function.
  • Increased maternal IGFBP-1 in FGR may be a consequence of impaired placental perfusion.
  • Elevated IGFBP-1 could reduce maternal IGF-I availability to the placenta, potentially exacerbating placental dysfunction and fetal growth restriction.
Abstract

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