RAEM REVISTA ARGENTINA DE
ENDOCRINOLOGÍA Y METABOLISMO
     
Volumen 52 #2 | Año 2015 Volver Indice
resumen Resumen abstract Abstract pdf PDF pdf PDF ENGLISH
 
  TRABAJO ORIGINAL
  Effect of Prenatal Hyperandrogenism on Fertility  
  Authors: Ferreira SR, Vélez LM, Motta AB  
     
  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 pubertal age. 2) To study the fertility of rats during adult life with and without gonadotropin stimulation.
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.

Rev Argent Endocrinol Metab 52:73-78, 2015
No financial conflicts of interest exist.
 
     
  Key words: prenatal hyperandrogenization, fertility, polycystic ovary syndrome  
 
 
 
 
 
 
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