Geburtshilfe Frauenheilkd 2018; 78(10): 123
DOI: 10.1055/s-0038-1671120
Poster
Donnerstag, 01.11.2018
Pränatal- und Geburtsmedizin I
Georg Thieme Verlag KG Stuttgart · New York

Placental uric acid transport system and its impact on fetal development

B Lüscher
1  Universitätsklinik für Frauenheilkunde Inselspital Bern, Geburtshilfe, Bern, Schweiz
,
D Surbek
1  Universitätsklinik für Frauenheilkunde Inselspital Bern, Geburtshilfe, Bern, Schweiz
,
P Schneider
1  Universitätsklinik für Frauenheilkunde Inselspital Bern, Geburtshilfe, Bern, Schweiz
,
M Baumann
1  Universitätsklinik für Frauenheilkunde Inselspital Bern, Geburtshilfe, Bern, Schweiz
› Author Affiliations
Further Information

Publication History

Publication Date:
20 September 2018 (online)

 

Introduction:

Uric acid is increased in women with pre-eclampsia and is believed to play a significant role in its pathogenesis. The main placental uric acid transporter is glucose transporter (GLUT)-9. In these studies we use of the novel GLUT9-knock out mouse model to investigate the placental uric acid system and its impact on fetal development.

Methods:

Female GLUT9(+/-) mice were mated with GLUT9(+/-) male mice. At gestational day 18.5 fetuses were sacrificed for blood sampling and measurement of uric acid serum levels, while in other pregnancies following birth the pups were daily weighted until day 70. At day 70 these mice were sacrificed and pancreas, liver and kidney were weighted and processed for histological analysis to assess potential abnormal organ development.

Results:

The GLUT9(-/-) fetuses showed a 3-fold increase in serum uric acid levels compared to GLUT9(+/-) and GLUT9(+/+) fetuses and their GLUT9(+/-) mothers. GLUT9(-/-) mice showed neonatal growth restriction compared to GLUT9(+/-) and GLUT9(+/+) mice. GLUT9(-/-) mice had decreased kidney mass by 25 ± 0.15% (mean ± SD, n = 7, p < 0.01, Student's t-test) and 35 ± 0.21% (n = 7, p < 0.01) for the left and the right kidney, respectively, compared to GLUT9(+/-) mice.

Conclusion:

These data show for the first time that in vivo uric acid is dependent on a specific uric acid transporter, i.e. GLUT9. Further there is strong evidence that fetal hyperuricemia is responsible for the observed impaired development of neonatal GLUT9(-/-) mice. Further studies investigating the potential links between hyperuricemia, altered placental function and metabolic fetal programming are eagerly needed.