ArticleHistochemistry1993
Immunohistochemical localization of glucose transporters and insulin receptors in human fetal membranes at term.
Article in Histochemistry, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 52 citations in OpenAlex.
- Placental expression of GLUT-1, GLUT-3, and GLUT-4 mRNA and transcriptome profiling in pregnant women with diabetes.Journal of diabetes investigation · 2025Article
- Feto-placental Unit: From Development to Function.Advances in experimental medicine and biology · 2023Review
- Fetomaternal Expression of Glucose Transporters (GLUTs)-Biochemical, Cellular and Clinical Aspects.Nutrients · 2022Review
- Placental adaptations in growth restriction.Nutrients · 2015Review
- Metastatic hepatocarcinoma he/de tumor model in rat.Journal of Cancer · 2014Article
- Article
- Overexpression of GLUT3 placental glucose transporter in diabetic rats.The Journal of clinical investigation · 1995Article
- Localisation of the high affinity facilitative glucose transporter protein GLUT 1 in the placenta of human, marmoset monkey (Callithrix jacchus) and rat at different developmental stages.Cell and tissue research · 1995Article
- Management of Dysglycemia in a Pregnancy Complicated by Fanconi-Bickel Syndrome.AACE clinical case reportsArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The localization has been investigated of the isoforms GLUT1, GLUT3 and GLUT4 of glucose transporter proteins as well as of insulin receptors. Fetal membranes (n = 10) were examined by immunohistochemical methods at the light and electron microscopic levels using mono- and polyclonal antibodies. In all amnion epithelial cells, GLUT1 and GLUT3 antibodies were bound to the apical membrane. Very rarely the GLUT1 antibody also immunostained the basolateral membrane and reacted weakly with the endomembrane system and membranes of the lateral cell protrusions. Fibroblasts reacted with the antibodies against GLUT1, GLUT4 and insulin receptor, whereas they were labelled only in one case with GLUT3 antibody. Cytotrophoblast cells were only stained with antibodies against GLUT1 and GLUT3. Antibodies against GLUT4 only reacted with fibroblasts in the membranes. On amnion epithelial cells, weak immunoreactivity with insulin receptor antibodies was detected only at the electron microscopic level. The data indicate: (1) GLUT1 is located on all cells of the amnion, whereas GLUT3 is present in detectable amounts only on amnion epithelial cells and cytotrophoblast; (2) GLUT1 and GLUT3 on amnion epithelial cells are predominantly located on the apical surface; (3) GLUT4 and insulin receptors are not regularly expressed. We suggest that amnion epithelial cells cover their basal glucose requirements from the amniotic fluid and not from the maternal circulation.
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