scholarly journals The Time of Prenatal Androgen Exposure Affects Development of Polycystic Ovary Syndrome-Like Phenotype in Adulthood in Female Rats

2014 ◽  
Vol 12 (2) ◽  
Author(s):  
Fahimeh Ramezani Tehrani ◽  
Mahsa Noroozzadeh ◽  
Saleh Zahediasl ◽  
Abbas Piryaei ◽  
Somayeh Hashemi ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Female Rats ◽  
Ovary Syndrome ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen

scholarly journals Origins and Impact of Psychological Traits in Polycystic Ovary Syndrome

2019 ◽  
Vol 7 (8) ◽  
pp. 86 ◽  
Author(s):  
Elisabet Stener-Victorin ◽  
Maria Manti ◽  
Romina Fornes ◽  
Sanjiv Risal ◽  
Haojiang Lu ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Anxiety Disorders ◽  
Maternal Obesity ◽  
Steroid Receptors ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Psychological Traits ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen

Women with polycystic ovary syndrome (PCOS) exhibit compromised psychiatric health. Independent of obesity, women with PCOS are more susceptible to have anxiety and depression diagnoses and other neuropsychiatric disorders. During pregnancy women with PCOS display high circulating androgen levels that may cause prenatal androgen exposure affecting the growing fetus and increasing the risk of mood disorders in offspring. Increasing evidence supports a non-genetic, maternal contribution to the development of PCOS and anxiety disorders in the next generation. Prenatal androgenized rodent models reflecting the anxiety-like phenotype of PCOS in the offspring, found evidence for the altered placenta and androgen receptor function in the amygdala, together with changes in the expression of genes associated with emotional regulation and steroid receptors in the amygdala and hippocampus. These findings defined a previously unknown mechanism that may be critical in understanding how maternal androgen excess can increase the risk of developing anxiety disorders in daughters and partly in sons of PCOS mothers. Maternal obesity is another common feature of PCOS causing an unfavorable intrauterine environment which may contribute to psychiatric problems in the offspring. Whether environmental factors such as prenatal androgen exposure and obesity increase the offspring’s susceptibility to develop psychiatric ill-health will be discussed.

scholarly journals Maternal polycystic ovary syndrome and risk of neuropsychiatric disorders in offspring: prenatal androgen exposure or genetic confounding?

2019 ◽  
Vol 50 (4) ◽  
pp. 616-624 ◽  
Author(s):  
Carolyn E. Cesta ◽  
Anna S. Öberg ◽  
Abraham Ibrahimson ◽  
Ikram Yusuf ◽  
Henrik Larsson ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Cox Regression ◽  
Polycystic Ovary ◽  
Neuropsychiatric Disorders ◽  
Autism Spectrum ◽  
Ovary Syndrome ◽  
Androgen Exposure ◽  
Increased Risk ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen

AbstractBackgroundMaternal polycystic ovary syndrome (PCOS) has been proposed as a model for investigating the role of prenatal androgen exposure in the development of neuropsychiatric disorders. However, women with PCOS are at higher risk of developing psychiatric conditions and previous studies are likely confounded by genetic influences.MethodsA Swedish nationwide register-based cohort study was conducted to disentangle the influence of prenatal androgen exposure from familial confounding in the association between maternal PCOS and offspring attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and Tourette's disorder and chronic tic disorders (TD/CTD). PCOS-exposed offspring (n = 21 280) were compared with unrelated PCOS-unexposed offspring (n = 200 816) and PCOS-unexposed cousins (n = 17 295). Associations were estimated with stratified Cox regression models.ResultsPCOS-exposed offspring had increased risk of being diagnosed with ADHD, ASD, and TD/CTD compared with unrelated PCOS-unexposed offspring. Associations were stronger in girls for ADHD and ASD but not TD/CTD [ADHD: adjusted hazard ratio (aHR) = 1.61 (95% confidence interval (CI) 1.31–1.99), ASD: aHR = 2.02 (95% CI 1.45–2.82)] than boys [ADHD: aHR = 1.37 (95% CI 1.19–1.57), ASD: aHR = 1.46 (95% CI 1.21–1.76)]. For ADHD and ASD, aHRs for girls were stronger when compared with PCOS-unexposed cousins, but slightly attenuated for boys.ConclusionsEstimates were similar when accounting for familial confounding (i.e. genetics and environmental factors shared by cousins) and stronger in girls for ADHD and ASD, potentially indicating a differential influence of prenatal androgen exposure v. genetic factors. These results strengthen evidence for a potential causal influence of prenatal androgen exposure on the development of male-predominant neuropsychiatric disorders in female offspring of women with PCOS.

scholarly journals Prenatal androgen exposure and transgenerational susceptibility to polycystic ovary syndrome

2019 ◽  
Vol 25 (12) ◽  
pp. 1894-1904 ◽  
Author(s):  
Sanjiv Risal ◽  
Yu Pei ◽  
Haojiang Lu ◽  
Maria Manti ◽  
Romina Fornes ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen

scholarly journals Excess Androgens in Utero Alters Fetal Testis Development

Endocrinology ◽  
2013 ◽  
Vol 154 (5) ◽  
pp. 1921-1933 ◽  
Author(s):  
Fiona Connolly ◽  
Michael T. Rae ◽  
Lilli Bittner ◽  
Kirsten Hogg ◽  
Alan S. McNeilly ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Leydig Cell ◽  
Polycystic Ovary ◽  
Developmental Trajectory ◽  
Testicular Development ◽  
Cell Distribution ◽  
Ovary Syndrome ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen

Abstract Prenatal androgenization induces a polycystic ovary syndrome-like phenotype in adult female offspring, which is associated with alterations that can be detected in the fetal ovary, suggesting gestational origins of this condition. We therefore investigated whether increased prenatal androgen exposure also altered testicular development using ovine animal models. Biweekly maternal testosterone propionate (TP; 100 mg) from day 62 to day 70/day 90 of gestation altered male developmental trajectory. In male fetuses serum LH was decreased (P < .01), and testicular STAR, CYP11, and CYP17 abundance were reduced. Coincident with this, basal testicular T synthesis was decreased in vitro (P < .001). Leydig cell distribution was severely perturbed in all testes prenatally exposed to TP (P < .001). To examine the contribution of estrogens, fetuses were injected with TP (20 mg), the potent estrogen agonist, diethylstilbestrol (DES; 20 mg), or vehicle control at day 62 and day 82 and assessed at day 90. The effects of fetal (direct) TP treatment, but not DES, paralleled maternal (indirect) TP exposure, supporting a direct androgen effect. Cessation of maternal androgenization at day 102 returned Leydig cell distribution to normal but increased basal T output, at day 112, demonstrating Leydig cell developmental plasticity. Earlier maternal androgen exposure from day 30 similarly influenced Leydig cell development at day 90 but additionally affected the expression of Sertoli and germ cell markers. We show in this study that increased prenatal androgen exposure alters development and function of Leydig cells at a time when androgen production is paramount for male development. This supports the concept that gestational antecedents associated with polycystic ovary syndrome may have effects on the male fetus.

scholarly journals Fetal programming of polycystic ovary syndrome: Effects of androgen exposure on prenatal ovarian development

2021 ◽  
Vol 207 ◽  
pp. 105830
Author(s):  
Maya Barsky ◽  
Jamie Merkison ◽  
Pardis Hosseinzadeh ◽  
Liubin Yang ◽  
Janet Bruno-Gaston ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Fetal Programming ◽  
Ovarian Development ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Androgen Exposure

scholarly journals The Pancreas Is Altered by In Utero Androgen Exposure: Implications for Clinical Conditions Such as Polycystic Ovary Syndrome (PCOS)

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e56263 ◽  
Author(s):  
Mick Rae ◽  
Cathal Grace ◽  
Kirsten Hogg ◽  
Lisa Marie Wilson ◽  
Sophie L. McHaffie ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
In Utero ◽  
Ovary Syndrome ◽  
Androgen Exposure ◽  
Clinical Conditions
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