Cited by 41Pregnancy and preeclampsia studiesReproductive Physiology in LivestockBirth, Development, and Health

Time-dependent physiological regulation of ovine placental GLUT-3 glucose transporter protein

Das, Utpala G., He, Jing, Ehrhardt, Richard A., Hay, William W., Devaskar, Sherin U.·2000·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

Abstract

We immunolocalized the GLUT-3 glucose transporter isoform versus GLUT-1 in the late-gestation epitheliochorial ovine placenta, and we examined the effect of chronic maternal hyperglycemia and hypoglycemia on placental GLUT-3 concentrations. GLUT-3 was limited to the apical surface of the trophoectoderm, whereas GLUT-1 was on the basolateral and apical surfaces of this cell layer and in the epithelial cells lining the placental uterine glands. GLUT-3 concentrations declined at 17–20 days of chronic hyperglycemia ( P < 0.05), associated with increased uterine and uteroplacental net glucose uptake rate, but a normal fetal glucose uptake rate was observed. Chronic hypoglycemia did not change GLUT-3 concentrations, although uterine, uteroplacental, and fetal net glucose uptake rates were decreased. Thus maternal hyperglycemia causes a time-dependent decline in the entire placental glucose transporter pool (GLUT-1 and GLUT-3). In contrast, maternal hypoglycemia decreases GLUT-1 but not GLUT-3, resulting in a relatively increased GLUT-3 contribution to the placental glucose transporter pool, which could maintain glucose delivery to the placenta relative to the fetus when maternal glucose is low.

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Crossref · 10.1152/ajpregu.2000.279.6.r2252

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  • 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 [138]

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Authors
Das, U. G., He, J., Ehrhardt, R. A., Hay, W. W., & Devaskar, S. U.
Affiliations
  • University of Pittsburgh (US)
  • Cornell University (US)
  • University of Colorado Anschutz (US)
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Published
2000-12-01
Volume
279
Issue
6
Pages
R2252-R2261
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
OpenAlex
W2200929671
Cited by
41
References
37
Citations by year
2024: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2016: 3 · 2015: 1 · 2014: 3 · 2013: 2 · 2012: 2
FWCI
4.27
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-33997, HD25024, R01HD028794, HD-28794, R01HD033997)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • 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
Keywords
GLUT3, GLUT1, glucose transporters, ovine placenta, maternal hyperglycemia, maternal hypoglycemia, trophectoderm, endometrial glands, gestation
MeSH terms
Animals, Blood Glucose, Female, Fetal Blood, Homeostasis, Hyperglycemia, Hypoglycemia, Maternal-Fetal Exchange, Monosaccharide Transport Proteins, Nerve Tissue Proteins, Placenta, Pregnancy, Pregnancy Complications, Sheep, Glucose Transporter Type 3

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