» Articles » PMID: 35631166

Fetomaternal Expression of Glucose Transporters (GLUTs)-Biochemical, Cellular and Clinical Aspects

Overview
Journal Nutrients
Date 2022 May 28
PMID 35631166
Authors
Affiliations
Soon will be listed here.
Abstract

Several types of specialized glucose transporters (GLUTs) provide constant glucose transport from the maternal circulation to the developing fetus through the placental barrier from the early stages of pregnancy. GLUT1 is a prominent protein isoform that regulates placental glucose transfer via glucose-facilitated diffusion. The GLUT1 membrane protein density and permeability of the syncytial basal membrane (BM) are the main factors limiting the rate of glucose diffusion in the fetomaternal compartment in physiological conditions. Besides GLUT1, the GLUT3 and GLUT4 isoforms are widely expressed across the human placenta. Numerous medical conditions and molecules, such as hormones, adipokines, and xenobiotics, alter the GLUT's mRNA and protein expression. Diabetes upregulates the BM GLUT's density and promotes fetomaternal glucose transport, leading to excessive fetal growth. However, most studies have found no between-group differences in GLUTs' placental expression in macrosomic and normal control pregnancies. The fetomaternal GLUTs expression may also be influenced by several other conditions, such as chronic hypoxia, preeclampsia, and intrahepatic cholestasis of pregnancy.

Citing Articles

Understanding glucose metabolism and insulin action at the blood-brain barrier: Implications for brain health and neurodegenerative diseases.

Zhu Y, Verkhratsky A, Chen H, Yi C Acta Physiol (Oxf). 2025; 241(2):e14283.

PMID: 39822067 PMC: 11737474. DOI: 10.1111/apha.14283.


Management of Dysglycemia in a Pregnancy Complicated by Fanconi-Bickel Syndrome.

Szmuilowicz E, Fruzyna E, Madden N, Bolden J, Kozek A, Vucko E AACE Clin Case Rep. 2024; 10(6):224-228.

PMID: 39734506 PMC: 11680753. DOI: 10.1016/j.aace.2024.07.008.


Supplementation with probiotics co-cultivation improves the reproductive performance in a sow-piglet model by mother-infant microbiota transmission and placental mTOR signaling.

Li S, Lu T, Lin Z, Zhang Y, Zhou X, Li M World J Microbiol Biotechnol. 2024; 41(1):13.

PMID: 39704872 DOI: 10.1007/s11274-024-04222-5.


Assessment of Changes in the Expression of Genes Involved in Insulin Signaling and Glucose Transport in Leukocytes of Women with Gestational Diabetes During Pregnancy and in the Postpartum Period.

Zieleniak A, Zurawska-Klis M, Laszcz K, Bulash K, Pacyga D, Cypryk K Int J Mol Sci. 2024; 25(23).

PMID: 39684804 PMC: 11641716. DOI: 10.3390/ijms252313094.


Placental expression of GLUT-1, GLUT-3, and GLUT-4 mRNA and transcriptome profiling in pregnant women with diabetes.

Sibiak R, Gutaj P, Mantaj U, Adamczak L, Blatkiewicz M, Rucinski M J Diabetes Investig. 2024; 16(3):543-554.

PMID: 39652454 PMC: 11871384. DOI: 10.1111/jdi.14369.


References
1.
Ermini L, Nuzzo A, Ietta F, Romagnoli R, Moretti L, Masturzo B . Placental Glucose Transporters and Response to Bisphenol A in Pregnancies from of Normal and Overweight Mothers. Int J Mol Sci. 2021; 22(12). PMC: 8233759. DOI: 10.3390/ijms22126625. View

2.
Zamudio S, Baumann M, Illsley N . Effects of chronic hypoxia in vivo on the expression of human placental glucose transporters. Placenta. 2005; 27(1):49-55. PMC: 4497571. DOI: 10.1016/j.placenta.2004.12.010. View

3.
Arnott G, Coghill G, McArdle H, Hundal H . Immunolocalization of GLUT1 and GLUT3 glucose transporters in human placenta. Biochem Soc Trans. 1994; 22(3):272S. DOI: 10.1042/bst022272s. View

4.
Zimmer D, Golichowski A, Karn C, Brechtel G, Baron A, Denne S . Glucose and amino acid turnover in untreated gestational diabetes. Diabetes Care. 1996; 19(6):591-6. DOI: 10.2337/diacare.19.6.591. View

5.
Janzen C, Lei M, Cho J, Sullivan P, Shin B, Devaskar S . Placental glucose transporter 3 (GLUT3) is up-regulated in human pregnancies complicated by late-onset intrauterine growth restriction. Placenta. 2013; 34(11):1072-8. PMC: 3843645. DOI: 10.1016/j.placenta.2013.08.010. View