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Cited by 120Birth, Development, and HealthPregnancy and preeclampsia studiesReproductive Physiology in Livestock

Nutritional Modulation of Adolescent Pregnancy Outcome – A Review

Wallace, J.M., Luther, J.S., Milne, J.S., Aitken, R.P., Redmer, D.A., Reynolds, L.P., Hay, W.W.·2006·Placenta
DOI 10.1016/j.placenta.2005.12.002
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Abstract

The risks of miscarriage, prematurity and low birth weight are particularly acute in adolescent girls who are still growing at the time of conception. The role of maternal nutrition in mediating pregnancy outcome in this vulnerable group has been examined in sheep models. When singleton bearing adolescent dams are overnourished to promote rapid maternal growth throughout pregnancy, growth of both the placenta and fetus is impaired, and birth occurs prematurely relative to control adolescents of equivalent age. Studies at mid-gestation, prior to alterations in placental mass, suggest that reduced proliferation of the fetal trophectoderm, impaired angiogenesis, and attenuated uteroplacental blood flows are early defects in placental development. By late pregnancy, relative placental mass is reduced by 45% but uteroplacental metabolism and placental glucose transfer capacity remain normal when expressed on a placental weight specific basis. The asymmetrically growth-restricted fetuses are hypoxic, hypoglycemic and have reduced insulin and IGF-1 concentrations. Absolute umbilical nutrient uptakes are attenuated but fetal utilisation of glucose, oxygen and amino acids remains normal on a fetal weight basis. This suggests altered sensitivities to metabolic signals and may have implications for subsequent metabolic health. At the other end of the nutritional spectrum, many girls who become pregnant have inadequate or marginal nutritional status during pregnancy. This situation is replicated in a second model whereby dams are prevented from growing during pregnancy by relatively underfeeding. Limiting maternal intake in this way gradually depletes maternal body reserves leading to a lower transplacental glucose gradient and a modest slowing of fetal growth in late pregnancy. These changes appear to be independent of alterations in placental growth per se. Thus, while the underlying mechanisms differ, maternal intake at both ends of the nutritional spectrum is a powerful determinant of fetal growth in pregnant adolescents.

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Crossref · 10.1016/j.placenta.2005.12.002

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38 of 38 references verified0 citation errors · 0 not checkable

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  • In some, but not all, studies these changes in placental vascularity are accompanied by decreases in cell proliferation, angiogenesis and uterine and/or umbilical blood flow.

    “In some, but not all, studies these changes in placental vascularity are accompanied by decreases in cell proliferation, angiogenesis and uterine and/or umbilical blood flow (166, 550, 557).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [557]

  • In sheep, changes in maternal glucose levels induced by fasting, over-nutrition or direct experimental manipulation by maternal glucose or insulin infusion alter uterine glucose uptake and, hence, placental consumption and transfer of glucose in relation to the transplacental glucose concentration gradient driving glucose flux.

    “In sheep, changes in maternal glucose levels induced by fasting, over-nutrition or direct experimental manipulation by maternal glucose or insulin infusion alter uterine glucose uptake and, hence, placental consumption and transfer of glucose in relation to the transplacental glucose concentration gradient driving glucose flux (247, 557).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [557]

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Authors
Wallace, J. M., Luther, J. S., Milne, J. S., Aitken, R. P., Redmer, D. A., Reynolds, L. P., & Hay, W. W.
Affiliations
  • North Dakota State University (US)
  • University of Colorado Health (US)
Corresponding author
Wallace, J.M.
ORCID
Venue
Placenta
Publisher
Elsevier BV
Published
2006-04
Volume
27
Pages
61-68
ISSN
0143-4004 (ISSN-L)
DOI
10.1016/j.placenta.2005.12.002
OpenAlex
W2063691670
Cited by
120
References
37
Citations by year
2026: 2 · 2025: 2 · 2024: 6 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 5 · 2018: 3 · 2017: 11 · 2016: 10 · 2015: 10 · 2014: 7 · 2013: 6 · 2012: 10
FWCI
0.99
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Placenta (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1r43hd020764-01)
  • National Heart, Lung, and Blood Institute (HL64141, R01HL064141)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-52138, R01DK052138)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 45784, HD20764, R01HD045784)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Life Sciences › Agricultural and Biological Sciences › Agronomy and Crop Science › Reproductive Physiology in Livestock
Keywords
adolescent pregnancy, maternal nutrition, fetal growth restriction, placental development, overnutrition, malnutrition, placental mass, fetal hypoxia, insulin-like growth factor I, uteroplacental blood flow, sheep model, birth weight, preterm birth, miscarriage
MeSH terms
Adolescent, Animals, Animal Nutritional Physiological Phenomena, Female, Fetal Growth Retardation, Humans, Placenta, Pregnancy, Pregnancy in Adolescence, Pregnancy Outcome, Sheep, Social Behavior, Uterus, Models, Animal, Maternal Nutritional Physiological Phenomena, Malnutrition, Fetal Development

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