Abstract

Intrauterine growth restriction (IUGR) is associated with reduced placental amino acid transport (AAT). However, it remains to be established if changes in AAT contribute to restricted fetal growth. We hypothesized that reduced in vivo placental AAT precedes the development of IUGR in baboons with maternal nutrient restriction (MNR). Baboons were fed either a control (ad libitum) or MNR diet (70% of control diet) from gestational day (GD) 30. At GD 140, in vivo transplacental AA transport was measured by infusing nine (13)C- or (2)H-labeled essential amino acids (EAAs) as a bolus into the maternal circulation at cesarean section. A fetal vein-to-maternal artery mole percent excess ratio for each EAA was measured. Microvillous plasma membrane (MVM) system A and system L transport activity were determined. Fetal and placental weights were not significantly different between MNR and control. In vivo, the fetal vein-to-maternal artery mole percent excess ratio was significantly decreased for tryptophan in MNR. MVM system A and system L activity was markedly reduced in MNR. Reduction of in vivo placental amino acid transport precedes fetal growth restriction in the non-human primate, suggesting that reduced placental amino acid transfer may contribute to IUGR.

Highlights

  • Introduction iationsIntrauterine growth restriction (IUGR) affects about 30 million babies each year worldwide and is a significant cause of perinatal morbidity and mortality [1,2,3]

  • We demonstrated that maternal protein restriction causes down-regulation of placental amino acid transport several days before fetal size reductions were observed [9,12]

  • We have developed a baboon model of 30% global caloric maternal nutrient restriction (MNR), which results in IUGR, reduced fetal circulating levels of essential amino acids, and structural and functional changes in a range of fetal organs [24,25,26,27,28,29,30,31,32,33] and long term increased risk for poor health

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Summary

Introduction

Intrauterine growth restriction (IUGR) affects about 30 million babies each year worldwide and is a significant cause of perinatal morbidity and mortality [1,2,3]. The failure of the normal increase in uteroplacental blood flow is believed to be the most common etiology of IUGR. Maternal undernutrition remains the leading cause of in utero restricted growth [7] in developing regions. Americans live in households experiencing food insecurity or hunger sometime during the year [8]. Exploring the effects of maternal undernutrition on placental function is highly relevant to many parts of the world where inadequate food intake in pregnant women is still a significant concern. Different etiologies of IUGR are Licensee MDPI, Basel, Switzerland

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