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.

Item Type:

Conference or Workshop Item (Abstract)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > Unit Childrens Hospital > Forschungsgruppe Pränatale Medizin
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Biochemistry and Molecular Medicine

UniBE Contributor:

Marini, Camilla; Lüscher, Benjamin; Jörger Messerli, Marianne; Sager, Ruth; Huang, Xiao; Gertsch, Jürg; Hediger, Matthias; Albrecht, Christiane; Baumann, Marc Ulrich and Surbek, Daniel

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISSN:

0143-4004

Publisher:

Elsevier

Language:

English

Submitter:

Barbara Järmann-Bangerter

Date Deposited:

02 Apr 2015 14:12

Last Modified:

02 Sep 2015 10:22

BORIS DOI:

10.7892/boris.67501

URI:

https://boris.unibe.ch/id/eprint/67501

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