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Cited by 58Reproductive Physiology in LivestockBirth, Development, and HealthPregnancy and preeclampsia studies

Upregulation of growth signaling and nutrient transporters in cotyledons of early to mid-gestational nutrient restricted ewes

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Ma, Y., Zhu, M.J., Uthlaut, A.B., Nijland, M.J., Nathanielsz, P.W., Hess, B.W., Ford, S.P.·2011·Placenta
DOI 10.1016/j.placenta.2011.01.007PMC PMC3049449
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Abstract

Multiparous ewes received 100% (control, C, n = 13) or 50% (nutrient restricted, NR, n = 14) of NRC dietary requirements from d28-d78 of gestation. On d78, 5 C and 6 NR ewes were necropsied. The remaining 8 C and 8 NR ewes were fed to 100% of NRC from d78-d135 and necropsied. Maternal blood was collected at both necropsies and at weekly intervals for assay of glucose, insulin and leptin. Fetal blood was collected at d78 and d135 necropsies for assay of glucose and lipids. Cotyledonary (COT) tissue was evaluated for protein and mRNA expression [fatty acid transporter (FATP)1, FATP4, CD36, glucose transporter (GLUT)1 and GLUT3], mRNA expression only [placenta fatty acid binding protein (FABPpm) and lipoprotein lipase (LPL)], or expression of phosphorylated and total protein forms [AMP kinase (AMPK)α, acetyl-CoA carboxylase (ACC), extracellular signal-regulated kinase (Erk)1/2, mammalian target of rapamycin (mTOR) and protein kinase B (Akt)]. On d78, but not d135, placental and fetal weights were reduced (P < 0.05) in NR vs. C ewes. Maternal circulating glucose, insulin and leptin levels were decreased in NR vs. C ewes on d78 (P < 0.05) but similar at d135. Fetal blood glucose and triglyceride levels were lower in NR vs. C ewes (P < 0.05) on d78, but similar on d135. On d78, GLUT1, FATP4, CD36 mRNA and protein expression levels, FABPpm mRNA level, and leptin protein level were all increased (P < 0.05) in COT of NR vs. C ewes. AMPK, ACC, and Erk1/2 activities were also increased (P < 0.05) in NR vs. C COT on d78. In contrast, only FATP4 was increased (P < 0.05) at both the mRNA and protein levels in COT of NR realimented vs. C ewes on d135. These data demonstrate placental adaptation to maternal NR through increasing nutrient transporter production and growth signaling activity.

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Crossref · 10.1016/j.placenta.2011.01.007

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  • No effect on mTOR signaling was observed at mid-to late-gestation in sheep fed 50% of the control diet.

    “However, no effect was observed at mid-to late-gestation in sheep fed 50% of the control diet (353).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [353]

  • Ovine placental GLUT expression is altered in response to longer term variations in maternal glycaemia with decreases in GLUT1 abundance in hypoglycaemia conditions, and in both GLUT1 and GLUT3 abundance in response to hyperglycaemia.

    “Ovine placental GLUT expression is altered in response to longer term variations in maternal glycaemia with decreases in GLUT1 abundance in hypoglycaemia conditions, and in both GLUT1”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [353]

  • Undernutrition of ewes from early to mid-gestation increases expression of several molecules involved in transplacental fatty acid transport at mid-gestation, although few of these changes persist until late gestation.

    “In addition, undernutrition of ewes from early to mid-gestation increases expression of several molecules involved in transplacental fatty acid transport at mid-gestation, although few of these changes persist until late gestation (353).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [353]

  • Dietary restriction during early to mid-gestation in ewes resulted in increased activation of AMPK in the fetal cotyledonary tissues at d78 but not later on d135, whereas over-nutrition resulted in the reverse.

    “Dietary restriction (50% of controls) during early to mid-gestation in ewes resulted in increased activation of AMPK in the fetal cotyledonary tissues at d78 but not later on d135 (353), whereas the reverse was the case with over-nutrition (150% of controls) (615).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [353]

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  1. [26]Council NR Nutrient Requirements of Sheep 1985 Washington DC National Academic Press

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Authors
Ma, Y., Zhu, M. J., Uthlaut, A. B., Nijland, M. J., Nathanielsz, P. W., Hess, B. W., & Ford, S. P.
Affiliations
University of Wyoming (US)
ORCID
Venue
Placenta
Publisher
Elsevier BV
Published
2011-03
Volume
32
Issue
3
Pages
255-263
ISSN
0143-4004 (ISSN-L)
DOI
10.1016/j.placenta.2011.01.007
PMC
PMC3049449
OpenAlex
W1974232929
Cited by
58
References
41
Citations by year
2026: 5 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 5 · 2021: 3 · 2020: 11 · 2019: 4 · 2018: 1 · 2017: 2 · 2016: 6 · 2015: 6 · 2014: 4 · 2013: 3 · 2012: 3
FWCI
6.78
Type
journal article
Language
en
Open access
Licence
Locations
  • Placenta (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • University of Wyoming
  • National Institutes of Health (2p20rr016474-09)
  • National Center for Research Resources (P20-RR-016474, 1P20RR16474)
Topics
  • Life Sciences › Agricultural and Biological Sciences › Agronomy and Crop Science › Reproductive Physiology in Livestock
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Keywords
maternal nutrient restriction, gestation, ewes, cotyledons, fetal growth, nutrient transporters, fatty acid transporters, glucose transporters, GLUT1, FATP4, CD36, FABPpm, lipoprotein lipase, AMPK, acetyl-CoA carboxylase, ERK1/2, mTOR, Akt, leptin
MeSH terms
Animals, Blood Glucose, Body Weight, Female, Fetus, Food Deprivation, Insulin, Male, Placenta, Pregnancy, Random Allocation, RNA, Messenger, Sheep, Blotting, Western, Signal Transduction, Up-Regulation, CD36 Antigens, Reverse Transcriptase Polymerase Chain Reaction, Fetal Weight, Leptin, Fatty Acid-Binding Proteins, Fatty Acid Transport Proteins, Glucose Transporter Type 1, Glucose Transporter Type 4

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