Endocrine Abstracts

Obesity epidemic is one of the major concerns in the world. Worryingly, a high percentage of pregnant women have obesity, which could imply several consequences. Maternal obesity leads to different abnormalities in pregnancy and delivery. In addition, recent studies show that the offspring of obese mothers has an increased probability to suffer cardiovascular, metabolic and reproductive diseases. We have previously demonstrated that exposure to a high fat diet is related to obesity, liver dysfunction, increased serum estradiol, advanced puberty and ovarian follicular alterations in the progeny. We aimed to determine if metformin prevents this developmental reprogramming produced by a high fat diet exposure. Sprague Dawley rats were distributed in three groups: Control diet (13% Kcal in fat); High Fat Diet (HF) (60% Kcal in fat, Research Diet, USA) and HF+ Metformin (60% Kcal in fat + metformin 150–200 mg/kg in tap water). Diet was administered for 1 month previous to pregnancy, during pregnancy and nursing. Metformin was administered from 1 week previous to pregnancy until weaning of the offspring. Metformin did not affect the weight gain during pregnancy and failed in prevent increased weight in offspring of obese mothers. At postnatal day (PND) 14 metformin tended to prevent the estradiol increase while at PND60 metformin significantly prevented the estradiol increase. Coherently, hepatic CYP3A2 (enzyme that metabolizes estradiol) decreased in offspring obese mothers and this decrease was prevented by metformin treatment. The generation of ovarian cyst was also prevented by metformin in offspring of obese mothers. In conclusion, metformin prevented some reproductive alterations triggered by maternal obesity on the offspring.