Journal of Glycobiology
Open Access

Metoclopramide-induced hyperprolactinemia changed on murine uterine

Glycobiology World Congress

August 10-12, 2015 Philadelphia, USA

Regina Celia Teixeira Gomes

Posters-Accepted Abstracts: J Glycobiol

Abstract :

Initially our group found out that the metoclopramide-induced hyperprolactinemia may negatively affect the endometrial
morphology. And in later studies we found out that the hyperprolactinemia caused a decrease in pinopode numbers and
embryo implantation in female mice thus interfering with the fertility and in ovarian function. In order to show the effectiveness
of treatment with 200 �¼g metoclopramide for 50 consecutive days, we measured the serum prolactin levels and also analyzed
the pituitary of animals. We proved that the hyperprolactinemia caused by metoclopramide in mice is due to an increase in
the number and activity of lactotrophs. The deepening of the research led us to several questions. What are the biochemical
changes that were occurring in the endometrial stroma (cells and extracellular matrix) of these animals? Finally, our results
showed that the elevation of prolactin may lead to changes in the amounts of glycosaminoglycans which are important for
embryo implantation in an animal model of hyperprolactinemia accompanied by a regular estrous cycle. Recently, we have
researched the gene expression of small leucine-rich proteoglycans (SLRPs) on the murine uterus non pregnant and pregnant
with hyperprolactinemia induced metoclopramide. The interactions between the production and degradation of these
substances with steroids and hyperprolactinemia is complex and difficult to explain because the signaling pathways involving
those hormones may influence the cell-cell and cell-extracellular matrix interactions in the endometrial stroma as well as they
may interfere with the appropriate preparation of the endometrium to receive the embryo.