Cited by 130Birth, Development, and HealthPregnancy and preeclampsia studiesGestational Diabetes Research and Management

Placental transport in response to altered maternal nutrition

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Gaccioli, F., Lager, S., Powell, T. L., Jansson, T.·2013·Journal of Developmental Origins of Health and Disease

Abstract

The mechanisms linking maternal nutrition to fetal growth and programming of adult disease remain to be fully established. We review data on changes in placental transport in response to altered maternal nutrition, including compromized utero-placental blood flow. In human intrauterine growth restriction and in most animal models involving maternal undernutrition or restricted placental blood flow, the activity of placental transporters, in particular for amino acids, is decreased in late pregnancy. The effect of maternal overnutrition on placental transport remains largely unexplored. However, some, but not all, studies in women with diabetes giving birth to large babies indicate an upregulation of placental transporters for amino acids, glucose and fatty acids. These data support the concept that the placenta responds to maternal nutritional cues by altering placental function to match fetal growth to the ability of the maternal supply line to allocate resources to the fetus. On the other hand, some findings in humans and mice suggest that placental transporters are regulated in response to fetal demand signals. These observations are consistent with the idea that fetal signals regulate placental function to compensate for changes in nutrient availability. We propose that the placenta integrates maternal and fetal nutritional cues with information from intrinsic nutrient sensors. Together, these signals regulate placental growth and nutrient transport to balance fetal demand with the ability of the mother to support pregnancy. Thus, the placenta plays a critical role in modulating maternal–fetal resource allocation, thereby affecting fetal growth and the long-term health of the offspring.

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  • The placenta acts as an environmental sensor, integrating signals of the current availability of oxygen and nutrients, maternal stores of nutrient reserves and of the fetal nutrient demands for growth driven by the genes and actual mass of the fetus.

    “Thus, the placenta acts as an environmental sensor, integrating signals of the current availability of oxygen and nutrients, maternal stores of nutrient reserves and of the fetal nutrient demands for growth driven by the genes and actual mass of the fetus (74,204).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [204]

  • Maternal nutrition is a major determinant of placental development and alters the morphological, transport and endocrine characteristics of the placenta with consequences for fetal nutrient supply in a wide range of species including laboratory and farm species as well as human and non-human primates.

    “In addition, maternal nutrition is a major determinant of placental development and alters the morphological, transport and endocrine characteristics of the placenta with consequences for the fetal nutrient supply in a wide range of species including laboratory and farm species as well as human and non-human primates (47, 144, 204, 522, 550).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [204]

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Authors
Gaccioli, F., Lager, S., Powell, T. L., & Jansson, T.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
Corresponding author
Jansson, T.
Venue
Journal of Developmental Origins of Health and Disease
Published
2012-07-31
Volume
4
Issue
2
Pages
101-115
ISSN
  • 2040-1744 (ISSN-L)
  • 2040-1752
OpenAlex
W2164709834
Cited by
129
References
177
Citations by year
2026: 13 · 2025: 7 · 2024: 7 · 2023: 12 · 2022: 10 · 2021: 13 · 2020: 11 · 2019: 7 · 2018: 10 · 2017: 15 · 2016: 8 · 2015: 7 · 2014: 4 · 2013: 4 · 2012: 1
FWCI
4.49
Type
journal article
Language
en
Open access
Locations
  • Journal of Developmental Origins of Health and Disease (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5r01hd068370-11)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK089989)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R21HD071306, R01-HD068370, R01HD065007)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
placental nutrient transport, maternal nutrition, fetal growth restriction, maternal undernutrition, maternal overnutrition, placental blood flow, amino acid transporters, glucose transport, fatty acid uptake, fetal programming, fetal growth, diabetes in pregnancy, placental development

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