Placental Glucose Transporter (GLUT1) Expression in Pre-Eclampsia

Marini, Camilla; Lüscher, Benjamin; Jörger Messerli, Marianne; Sager, Ruth; Huang, Xiao; Gertsch, Jürg; Hediger, Matthias; Albrecht, Christiane; Baumann, Marc Ulrich; Surbek, Daniel (March 2014). Placental Glucose Transporter (GLUT1) Expression in Pre-Eclampsia. Reproductive sciences, 21(3), 304A-304A. Sage

Text 6.pdf - Published Version Restricted to registered users only Available under License Publisher holds Copyright. Download (439kB)

Placental Glucose Transporter (GLUT1) Expression in Pre-
Eclampsia.
INTRODUCTION: Glucose is the most important substrate for fetal
growth. Indeed, there is no significant de novo glucose synthesis in
the fetus and the fetal up-take of glucose rely on maternal supply and
transplacental transport. Therefore, a defective placental transporter
system may affect the intrauterine environment compromising fetal as
well as mother well-being. On this line, we speculated that the placental
glucose transport system could be impaired in pre-eclampsia (PE).
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. mRNA
levels were quantified by quantitative real-time PCR. A radiolabeled
substrate up-take assay was established to assess glucose transport activity.
FACS analysis was performed to check the shape of MVM. Statistical
analysis was performed using one way ANOVA test.
RESULTS: GLUT1 protein levels were down-regulated (70%; P<0.01)
in pre-eclamptic placentae when compared to control placentae. This data
is in line with the reduced glucose up-take in MVM prepared from preeclamptic
placentae. Of note, the mRNA levels of GLUT1 did not change
between placentae affected by PE and normal placentae, suggesting that
the levels of GLUT1 are post-transcriptionally regulated. FACS analysis
on MVM vesicles from both normal placentae and pre-eclamptic placentae
showed equal heterogeneity in the complexes formed. This excluded the
possibility that the altered glucose up-take observed in pre-eclamptic
MVM was caused by a different shape of these vesicles.
CONCLUSIONS: Protein and functional studies of GLUT1 in MVM
suggest that in pre-eclampsia the glucose transport between mother and
fetus might be defective. To further investigate this important biological
aspect we will increase the number of samples obtained from patients
and use primary cells to study trans epithelial transport system in vitro.

Interest & Impact

Downloads

2 since deposited on 02 Apr 2015
0 in the past 12 months

Citations

5 Citations in Web of Science ®
6 Citations in Scopus

Search

in Google Scholar™

Services

Actions (login required)

Edit item

Actions (login required)

Edit item