Placental glucose transporter (GLUT)-1 is down-regulated in preeclampsia

• Published in: Placenta (Eastbourne) 2017-07, Vol.55, p.94-99
• Main Authors: Lüscher, Benjamin P., PhD, Marini, Camilla, Joerger-Messerli, Marianne, Huang, Xiao, Hediger, Matthias A, Albrecht, Christiane, Surbek, Daniel V, Baumann, Marc U
• Format: Article
• Language: English
• Subjects: Adult; Case-Control Studies; Cell Membrane - metabolism; Down-Regulation; Female; Glucose transport; Glucose Transporter Type 1 - metabolism; GLUT1; Humans; Internal Medicine; Obstetrics and Gynecology; Placenta; Placenta - metabolism; Pre-Eclampsia - metabolism; Preeclampsia; Pregnancy; Syncytiotrophoblast
• ISSN: 0143-4004; 1532-3102
• DOI: 10.1016/j.placenta.2017.04.023

Abstract Introduction Transplacental fetal glucose supply is predominantly regulated by glucose transporter-1 (GLUT1). Altered expression and/or function of GLUT1 may affect the intrauterine environment, which could compromise fetal development and may contribute to fetal programming. To date it is unknown whether placental GLUT1 is affected by preeclampsia, which is often associated with intrauterine growth restriction (IUGR). We addressed the hypothesis that preeclampsia leads to decreased expression and function of placental GLUT1. Methods Placentae were obtained following normal pregnancy and from pregnancies affected by preeclampsia. Washed villous tissue fragments were used to prepare syncytial microvillous (MVM) and basal plasma membranes (BM) microvesicles. GLUT1 protein and mRNA expression was assessed by Western blot analysis and qPCR using Fast SYBR Green. Radio-labeled glucose up-take assay using placenta-derived syncytial microvesicles was used to analyze GLUT1 function. Results GLUT1 protein expression was significantly down-regulated in (apical) MVM of the syncytiotrophoblast in preeclampsia (n = 6) compared to controls (n = 6) (0.40 ± 0.04 versus 1.00 ± 0.06, arbitrary units, P