ECE2015 Eposter Presentations Reproduction, endocrine disruptors and signalling (92 abstracts)
Maternal obesity in pregnant rats is associated to increased levels of oestradiol during early postnatal life and altered ovarian follicular development in the offspring
Aldo Reyes 1 , Luisa Ramírez 1 , Valery Ambrosetti 1 , Marcelo Guerra 1 , Daniela Álvarez 1 , Sofía Olguín 1 , Daniela Fernandois 2 , Ramón Sotomayor-Zárate 3 & Gonzalo Cruz 1
1Laboratorio de Alteraciones Reproductivas y Metabólicas, CNPC, Facultad de Ciencias, Instituto de Fisiología, Universidad de Valparaíso, Valparaíso/Valparaíso, Chile; 2Programa de Doctorado en Farmacología, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago/Santiago, Chile; 3Laboratorio de Neuroquímica y Neurofarmacología, CNPC, Facultad de Ciencias, Instituto de Fisiología, Universidad de Valparaíso, Valparaíso/Valparaíso, Chile.
Obesity during gestation has been related to predisposition to endocrine and metabolic diseases in the offspring. Regarding reproductive effects, an increase in BMI in pregnant mothers is associated with precocious puberty in their offspring. This has been replicated in animal models of high fat diet (HFD) administration to mothers. Also, gestational obesity has been associated to higher susceptibility to developing breast cancer in the offspring. As both precocious puberty and breast cancer are strongly related to higher oestrogens levels, we studied if offspring of rats exposed to a HFD had increased levels of endogenous oestradiol from neonatal until adult age. In addition, we evaluated ovarian follicular development in adult rats because early exposure to oestrogens alters ovarian follicular development. Twenty-four Sprague–Dawley rats were fed with HFD (60% kcal fat, Research Diet) and control diet (12% kcal fat, Champion) 1 month previous to pregnancy, during pregnancy and during nursing. Offspring rats were killed at postnatal day (PND) 1, PND7, PND14, PND30, and PND60. We found that offspring of obese mothers had an increase in body weight from PND1 until PND60, and they had an early vaginal opening indicating precocious puberty. At PND60 the offspring of obese mothers showed less antral follicles and appearance of follicular cyst in the ovary. Female offspring of obese mothers had an increase in serum levels of oestradiol at PND1, PND7, PND14, PND30, and PND60. We also found a decrease in the expression of hepatic cyp3a in offspring of obese mothers in concordance with clear signs of hepatic steatosis. We conclude that maternal obesity alters hepatic metabolism of oestradiol in the offspring leading to increased levels of endogenous oestradiol. In addition, the increase in oestradiol levels during early postnatal development may be responsible of altered reproductive function in the offspring of obese mothers.
Disclosure: FONDECYT grant number 11130707.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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