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Revista argentina de endocrinología y metabolismo
versão On-line ISSN 1851-3034
Resumo
FERREIRA, SR; VELEZ, LM e MOTTA, AB. Effect of Prenatal Hyperandrogenism on Fertility. Rev. argent. endocrinol. metab. [online]. 2015, vol.52, n.2, pp.73-78. ISSN 1851-3034.
Introduction: Polycystic ovary syndrome (PCOS) is a common endocrine-reproductive disorder that affects women in their reproductive age. Prenatal hyperandrogenism is able to induce polycystic ovary syndrome (PCOS) in rats. PCOS is the commonest cause of anovulatory infertility. PCOS is not only a reproductive pathology, since it includes metabolic disorders (insulin resistance, impaired glucose tolerance, type 2 diabetes mellitus, high risk factor for cardiovascular diseases) and psychological symptoms (depression, increased anxiety, low self-esteem). However; the pathophysiology of PCOS is complex and remains unclear. Objectives: 1) To evaluate how hyperandrogenism (HA) affects the function of the uterine tissue at puber Pregnant Sprague-Dawley rats were prenatally injected daily with 2 mg free testosterone (HA group) or vehicle (Control group) from day 16 to day 19 of gestation. Female offspring were study at pubertal and adult age. The uterine oxidative stress was quantified by lipid peroxidation index (LP) and antioxidant glutathione (GSH) content. No differences were found between LP and GSH. The protein expressions of peroxisome proliferator-activated receptor gamma (PPAR γ), and the limiting enzyme of the PG synthesis, cyclooxygenase 2 (COX2) and the uterine PGE content increased in the HA group with respect to the C group. We also studied fertility at adult stage with and without hormone induction. The fertility rate decreased in HA. Hormone induction reversed the fertility rate similarly to controls. Conclusions: HA affects the uterine function in PCOS. HA increases protein levels of PPAR gamma, which modulates the pro-inflammatory status. The uterine oxidative stress was balanced. Fertility was decreased in the HA group and this was reversed by gonadotropin stimulation.
Palavras-chave : Prenatal hyperandrogenization; Fertility; Polycystic ovary syndrome.
