Maternal obesity impairs uterine contractile activity prior to implantation

BAZZANO, MV; ELIA EVELIN MARIEL; SARRIBLE, GB; BERÓN DE ASTRADA MARTÍN

Jornada; XX Jornadas Anuales de la Sociedad Argentina de Biología (SAB)-XVII Jornadas de la Sociedad Uruguaya de Biociencias (SUB), Segundas Jornadas Rioplatenses de Biología; 2018

 Obesity leads to several reproductive disorders. Using cafeteria diet(CAF)-induced obesity as animal model, we showed that the uterine β2 adrenergicreceptor (β2AR) expression is increased and embryo distribution is altered byobesity prior to implantation. β2AR signaling has a critical role in embryopositioning by controlling myometrial relaxation. The aim of the present study wasto determine whether obesity alters the uterine contractile activity and if itis due to the β2AR signaling disruption. Twenty two days old female wistar rats were divided into 2 groupsthat were fed ad libitum during 60days with: standard rodent chow (Controls) and CAF (Obeses). Then, rats were mated, euthanizedon 4.5gd (pre-implantation) and the uterine contractile activity was analyzed. Frequencyof the spontaneous uterine contractions was similar between uteri from controland obese rats. However, the amplitude of theses contractions were higher inobese rats compared to controls (p<0.01 and p<0.05). The uterinecontractile response to Salbutamol (0.05-500 ng/mL), a selective β2AR agonist,differed between groups. Despite it was decreased in response to Salbutamol in both groups; uteri from obese rats showed a reduction inthe amplitude of the curves in response to 0.5 ng/mL Salbutamol, while it wasobserved for 5 ng/mL in controls. These results demonstrate that thespontaneous uterine contractile activity is increased by obesity despite the higheruterine β2AR levels, suggestingthat the increase in the uterine β2AR expression could be a compensatory mechanismin response to the higher spontaneous uterine contractibility detected in theobese group. We conclude that obesity alters the uterine peristalsis and thismay lead to the disruption in the intrauterine embryo spacing observed in theseanimals. Moreover, and since the uterus must be relaxed for embryo nidation,these alterations may impair embryo implantation.