Poster Presentation Annual Meetings of the Endocrine Society of Australia and Society for Reproductive Biology and Australia and New Zealand Bone and Mineral Society 2016

Glucose transporter 1 (GLUT1) activity during implantation in normal and ovarian hyperstimulated rats (#470)

Vie Nguyen 1 , Laura Lindsay 1 , Christopher Murphy 1
  1. University Of Sydney, Sydney, NSW, Australia

Ovarian hyperstimulation (OH) is a technique used in assisted reproductive techniques such as in vitro fertilization (IVF) and has been shown to decrease endometrial receptivity for the implanting blastocyst. The factors which cause this decrease in uterine receptivity remain unclear.Glucose transporters (GLUTs) are a group of proteins that mediate glucose absorption from the blood stream into tissues and are important in pregnancy because they mediate glucose transport into the uterus which is a key factor in priming the uterus for implantation. Glucose is a necessary substrate for the Pentophosphate Pathway, which is the key energy utilization pathway for decidualisation. Without the requisite glucose, decidualisation cannot occur and this may account for low implantation rates in OH pregnancies.

To induce OH, female rats with regular oestrous cycles were given IP injections of 20IU of PMSG, then 20IU of HcG 24 hours later and mated overnight. Rat uterine tissue was collected at the times of implantation in normal and OH pregnancy. The tissue was analysed using western blotting techniques and immunofluorescence microscopy.

In normal pregnancy, GLUT1 is localized basal-laterally in the uterine epithelium but becomes diffuse at the time of implantation. The change in staining was not observed for OH pregnancies on the same days which suggest that the abnormal localisation of GLUT1 could ultimately lead to abnormal decidualisation. There was a significant increase in GLUT1 abundance in isolated uterine epithelial cells in OH pregnancy at the time of implantation when compared to normal pregnancy.The increase of GLUT1 abundance in OH pregnancy may suggest the overcompensation of the GLUT1 uniporter to account for the possible lack of glucose in the endometrium.  Hence, the lack of glucose as suggested by the overcompensation of GLUT1 abundance and abnormal localization observed in OH pregnancies may disrupt decidualisation which could adversely affect implantation.