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Cited by 96Pregnancy and preeclampsia studiesGestational Diabetes Research and ManagementBirth, Development, and Health

Time-dependent physiological regulation of rodent and ovine placental glucose transporter (GLUT-1) protein

Das, Utpala G., Sadiq, H. Farouk, Soares, Michael J., Hay, William W., Devaskar, Sherin U.·1998·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
DOI 10.1152/ajpregu.1998.274.2.r339
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Abstract

To examine the in vivo and in vitro time-dependent effects of glucose on placental glucose transporter (GLUT-1) protein levels, we employed Western blot analysis using placenta from the short-term streptozotocin-induced diabetic pregnancy (STZ-D), uterine artery ligation-intrauterine growth restriction (IUGR) rat models, pregnant sheep exposed to chronic maternal glucose and insulin infusions, and the HRP.1 rat trophoblastic cell line exposed to differing concentrations of glucose. In the rat, 6 days of STZ-D with maternal and fetal hyperglycemia caused no substantive change, whereas 72 h of IUGR with fetal hypoglycemia and ischemic hypoxia resulted in a 50% decline in placental GLUT-1 levels ( P < 0.05). In late-gestation ewes, maternal and fetal hyperglycemia caused an initial threefold increase at 48 h ( P< 0.05), with a persistent decline between 10 to 21 days, whereas maternal and fetal hypoglycemia led to a 30–50% decline in placental GLUT-1 levels ( P < 0.05). Studies in vitro demonstrated no effect of 0 mM, whereas 100 mM glucose caused a 60% decline ( P < 0.05; 48 h) in HRP.1 GLUT-1 levels compared with 5 mM of glucose. The added effect of hypoxia on 0 and 100 mM glucose concentrations appeared to increase GLUT-1 concentrations compared with normoxic cells ( P < 0.05; 100 mM at 18 h). We conclude that abnormal glucose concentrations alter rodent and ovine placental GLUT-1 levels in a time- and concentration-dependent manner; hypoxia may upregulate this effect. The changes in placental GLUT-1 concentrations may contribute toward the process of altered maternoplacentofetal transport of glucose, thereby regulating placental and fetal growth.

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Crossref · 10.1152/ajpregu.1998.274.2.r339

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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 [139]

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Authors
Das, U. G., Sadiq, H. F., Soares, M. J., Hay, W. W., & Devaskar, S. U.
Affiliations
  • University of Pittsburgh (US)
  • Cardinal Glennon Children’s Medical Center (US)
  • University of Kansas Medical Center (US)
  • University of Colorado Anschutz (US)
ORCID
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher
American Physiological Society
Published
1998-02-01
Volume
274
Issue
2
Pages
R339-R347
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
DOI
10.1152/ajpregu.1998.274.2.r339
OpenAlex
W2181380156
Cited by
96
References
33
Citations by year
2026: 1 · 2024: 4 · 2023: 1 · 2022: 1 · 2020: 4 · 2019: 3 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 2 · 2014: 2 · 2013: 5 · 2012: 4
FWCI
6.56
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
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Keywords
glucose transporters, placental glucose transport, maternal hyperglycemia, fetal hypoglycemia, fetal growth restriction, streptozotocin-induced diabetes, hypoxia, trophoblast, sheep pregnancy, rat pregnancy, fetal growth regulation
MeSH terms
Animals, Arteries, Cells, Cultured, Diabetes Mellitus, Experimental, Female, Fetal Growth Retardation, Glucose, Ligation, Monosaccharide Transport Proteins, Placenta, Pregnancy, Pregnancy in Diabetics, Sheep, Time Factors, Trophoblasts, Uterus, Blotting, Western, Rats, Sprague-Dawley, Glucose Transporter Type 1, Rats

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