INTRAUTERINE EMBRYO SPACING IS DISRUPTED BY OBESITY DURING THE PRE-IMPLANTATION PERIOD IN RATS.

BAZZANO MARÍA VICTORIA; PAZ DANTE AGUSTÍN; ELIA EVELIN MARIEL

Woods Hole

Simposio; 20th Frontiers in Reproduction SYMPOSIUM; 2017

Marine Biological Laboratory

The prevalence of obesity is increasing worldwide. It is related to several reproductive disorders including implantation problems. Aberrant embryo implantation causes, several times, pregnancy loss, a serious social and medical issue. So, diverse signaling pathways, including adrenergic receptor beta 2 (β2AR), control intrauterine embryo positioning so that implantation can correctly occur. However, whether and how the process of embryo implantation is affected by obesity remained elusive. Using cafeteria diet-induced obesity as animal model, we found that obesity causes aberrant uterine fetal spacing and macrosomia on gestation day (gd) 18.5. To elucidate whether this aberrant distribution is consequence of fetal reabsorptions or due to alterations in the foregoing embryo spacing, we analyzed the post implantation loss rates (PIL) and embryo positions just after (gd5.5) and before implantation (gd4.5). β2AR expression (qPCR and western blot) and localization (immunofluorescence) were analyzed on gd4.5. PIL was similar in control and obese rats; however aberrant uterine embryo spacing was detected on gd5.5 and gd4.5 in obese animals, indicating that obesity alters embryo positioning before implantation. On gd4.5, the total number of embryos (p