PLACENTAL GLUCOSE TRANSPORTER (GLUT)-1 REGULATION IN PREECLAMPSIA

Marini, Camilla; Lüscher, Benjamin; Jörger Messerli, Marianne; Sager, Ruth; Huang, Xiao; Gertsch, Jürg; Hediger, Matthias; Albrecht, Christiane; Baumann, Marc Ulrich; Surbek, Daniel (September 2014). PLACENTAL GLUCOSE TRANSPORTER (GLUT)-1 REGULATION IN PREECLAMPSIA. Placenta, 35, A83-A84. Elsevier

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PLACENTAL GLUCOSE TRANSPORTER (GLUT)-1 REGULATION IN PREECLAMPSIA
Camilla Marini a,b, Benjamin P. Lüscher a,b, Marianne J€orger-Messerli a,b, Ruth
Sager a,b, Xiao Huang c, Jürg Gertsch c, Matthias A. Hediger c, Christiane
Albrecht c, Marc U. Baumann a,c, Daniel V. Surbek a,c a Department of
Obstetrics and Gynecology, University Hospital of Bern, Bern, Switzerland,
Switzerland; b Department of Clinical Research, University of Bern, Bern,
Switzerland, Switzerland; c Institute for Biochemistry and Molecular Medicine,
University of Bern, Bern, Switzerland, Switzerland

Objectives: Glucose is a primary energy source for the fetus. The absence
of significant gluconeogenesis in the fetus means that the fetal up-take of
this vital nutrient is dependent on maternal supply and subsequent
transplacental transport. Altered expression and/or function of placental
transporters may affect the intrauterine environment and could compromise
fetal and mother well-being. We speculated that pre-eclampsia (PE)
impairs the placental glucose transport system.
Methods: Placentae were obtained after elective caesarean sections
following normal pregnancies and pre-eclamptic pregnancies. Syncytial
basal membrane (BM) and apical microvillus membrane (MVM) fractions
were prepared using differential ultra-centrifugation and magnesium
precipitation. Protein expression was assessed by western blot analysis.
mRNA levels in whole villous tissue lysate were quantified by real-time
PCR. To assess glucose transport activity a radiolabeled substrate up-take
assay and a transepithelial transport model using primary cytotrophoblasts
were established.
Results: GLUT1 mRNA expression was not changed in PE when compared
to control, whereas protein expression was significantly down-regulated.
Glucose up-take into syncytial microvesicles was reduced in PE compared to control. In a transepithelial transport model, phloretinmediated
inhibition of GLUT1 at the apical side of primary cytotrophoblasts
showed a 44% of reduction of transepithelial glucose transport at
IC50.
Conclusions: GLUT1 is down-regulated on protein and functional level in
PE compared to control. Altering glucose transport activity by inhibition of
apical GLUT-1 indicates that transplacental glucose transport might be
regulated on the apical side of the syncytiotrophoblast. These results might
help to understand better the regulation of GLUT1 transporter and maybe
in future to develop preventive strategies to modulate the fetal programming
and thereby reduce the incidence of disease for both the mother and
her child later in life.

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