Periconceptional Undernutrition Alters Growth Trajectory and Metabolic and Endocrine Responses to Fasting in Late-Gestation Fetal Sheep
Abstract
Maternal undernutrition during pregnancy can lead to impaired metabolic regulation in postnatal offspring. The extent to which such abnormalities are determined in early gestation, and may already be present in fetal life, is unknown. We studied the effect of periconceptional undernutrition on fetal growth and metabolism in late gestation. Ewes were either well fed throughout pregnancy (N) or undernourished to reduce ewe weight by 15% from 61 d before until 30 d after mating (UN). At 121 d, one cohort of ewes and their singleton fetuses (N, n=10; UN, n=10) were fasted for 72 h, given 25 g of glucose i.v. over 8 h, and refed. Fetal and placental weights were not different at 131 d. UN ewes had higher glucose, amino nitrogen, and Hb concentrations than N ewes. UN fetuses had higher glucose and lactate, and lower amino nitrogen and O2 concentrations and pH. UN ewes had higher insulin and lower IGF-I concentrations, and UN ewes and fetuses had higher placental lactogen concentrations. A second cohort (N, n=8; UN, n=10) were studied until term. Chest girth increment was reduced in UN fetuses until delivery, but birth weights were not significantly reduced. These findings suggest that fetal growth, metabolic and endocrine status, and placental function in late gestation are influenced by maternal nutrition in the periconceptional period, independent of fetal size. Metabolic and endocrine adaptations in the mother may mediate some of these effects. Such adaptations may allow continued fetal growth and survival in the face of a potentially adverse nutritional environment.
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Production of ovine placental lactogen (oPL) is nutritionally responsive and is increased in late gestation by short-term fasting and periconceptional undernutrition.
“In addition, production of ovine placental lactogen (oPL) is nutritionally responsive and is increased in late gestation by short-term fasting and periconceptional undernutrition (421, 422).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [422]
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Placental Origins of Chronic Disease
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- Authors
- Oliver, M. H., Hawkins, P., & Harding, J. E.
- Affiliations
- University of Auckland (NZ)
- Corresponding author
- Oliver, Mark H
- Venue
- Pediatric Research
- Published
- 2005-04
- Volume
- 57
- Issue
- 4
- Pages
- 591-598
- ISSN
- 0031-3998 (ISSN-L)
- 1530-0447
- OpenAlex
- W1971172689
- Cited by
- 107
- References
- 47
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 5 · 2017: 6 · 2016: 4 · 2015: 4 · 2014: 5 · 2013: 7 · 2012: 8
- FWCI
- 8.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pediatric Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Health Research Council of New Zealand
- 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
- maternal nutrition, fetal growth, fasting, glucose metabolism, insulin, insulin-like growth factor I, placental lactogen, placental function, fetal hypoxia, lactate, amino nitrogen, fetal sheep, gestation, birth weight, metabolic programming
- MeSH terms
- Animals, Birth Weight, Blood Chemical Analysis, Body Weight, Endocrine Glands, Fasting, Female, Fetus, Gestational Age, Glucose, Placenta, Pregnancy, Pregnancy, Animal, Cohort Studies, Sheep, Domestic, Maternal Nutritional Physiological Phenomena, Malnutrition
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