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. 2013 Apr 28;109(8):1382-8.
doi: 10.1017/S0007114512003261. Epub 2012 Oct 9.

Effect of 30% nutrient restriction in the first half of gestation on maternal and fetal baboon serum amino acid concentrations

Affiliations

Effect of 30% nutrient restriction in the first half of gestation on maternal and fetal baboon serum amino acid concentrations

Thomas J McDonald et al. Br J Nutr. .

Abstract

Mechanisms linking maternal nutrient restriction (MNR) to intra-uterine growth restriction (IUGR) and programming of adult disease remain to be established. The impact of controlled MNR on maternal and fetal amino acid metabolism has not been studied in non-human primates. We hypothesised that MNR in pregnant baboons decreases fetal amino acid availability by mid-gestation. We determined maternal and fetal circulating amino acid concentrations at 90 d gestation (90dG, term 184dG) in control baboons fed ad libitum (C, n 8) or 70% of C (MNR, n 6). Before pregnancy, C and MNR body weights and circulating amino acids were similar. At 90dG, MNR mothers had lower body weight than C mothers (P< 0·05). Fetal and placental weights were similar between the groups. MNR reduced maternal blood urea N (BUN), fetal BUN and fetal BUN:creatinine. Except for histidine and lysine in the C and MNR groups and glutamine in the MNR group, circulating concentrations of all amino acids were lower at 90dG compared with pre-pregnancy. Maternal circulating amino acids at 90dG were similar in the MNR and C groups. In contrast, MNR fetal β-alanine, glycine and taurine all increased. In conclusion, maternal circulating amino acids were maintained at normal levels and fetal amino acid availability was not impaired in response to 30% global MNR in pregnant baboons. However, MNR weight gain was reduced, suggesting adaptation in maternal-fetal resource allocation in an attempt to maintain normal fetal growth. We speculate that these adaptive mechanisms may fail later in gestation when fetal nutrient demands increase rapidly, resulting in IUGR.

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Conflict of interest statement

The authors declare that there is no conflict of interest.

References

    1. Walker SP, Wachs TD, Gardner JM, et al. Child development: risk factors for adverse outcomes in developing countries. Lancet. 2007;369:145–157. - PubMed
    1. Sankaran S, Kyle PM. Aetiology and pathogenesis of IUGR. Best Pract Res Clin Obstet Gynaecol. 2009;23:765–777. - PubMed
    1. Armitage JA, Khan IY, Taylor PD, et al. Developmental programming of the metabolic syndrome by maternal nutritional imbalance: how strong is the evidence from experimental models in mammals? J Physiol. 2004;561:355–377. - PMC - PubMed
    1. Wu G, Bazer FW, Cudd TA, et al. Maternal nutrition and fetal development. J Nutr. 2004;134:2169–2172. - PubMed
    1. Flynn NE, Meininger CJ, Haynes TE, et al. The metabolic basis of arginine nutrition and pharmacotherapy. Biomed Pharmacother. 2002;56:427–438. - PubMed

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