Developmental Programming of Polycystic Ovary Syndrome: Role of Prenatal Androgen Excess

2009 ◽  
pp. 83-103 ◽  
Author(s):  
Agathocles Tsatsoulis
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Developmental Programming ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Prenatal Androgen

scholarly journals A Narrative Review of Placental Contribution to Adverse Pregnancy Outcomes in Women With Polycystic Ovary Syndrome

2019 ◽  
Vol 104 (11) ◽  
pp. 5299-5315 ◽  
Author(s):  
Angela S Kelley ◽  
Yolanda R Smith ◽  
Vasantha Padmanabhan
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Pregnancy Complications ◽  
Polycystic Ovary ◽  
Evidence Synthesis ◽  
Developmental Programming ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Increased Risk ◽  
Adverse Pregnancy

Abstract Context Polycystic ovary syndrome (PCOS) is the most common endocrinopathy of reproductive-aged women. In pregnancy, women with PCOS experience increased risk of miscarriage, gestational diabetes, preeclampsia, and extremes of fetal birth weight, and their offspring are predisposed to reproductive and cardiometabolic dysfunction in adulthood. Pregnancy complications, adverse fetal outcomes, and developmental programming of long-term health risks are known to have placental origins. These findings highlight the plausibility of placental compromise in pregnancies of women with PCOS. Evidence Synthesis A comprehensive PubMed search was performed using terms “polycystic ovary syndrome,” “placenta,” “developmental programming,” “hyperandrogenism,” “androgen excess,” “insulin resistance,” “hyperinsulinemia,” “pregnancy,” and “pregnancy complications” in both human and animal experimental models. Conclusions There is limited human placental research specific to pregnancy of women with PCOS. Gestational androgen excess and insulin resistance are two clinical hallmarks of PCOS that may contribute to placental dysfunction and underlie the higher rates of maternal–fetal complications observed in pregnancies of women with PCOS. Additional research is needed to prevent adverse maternal and developmental outcomes in women with PCOS and their offspring.

scholarly journals Neuroendocrine Impairments of Polycystic Ovary Syndrome

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2230-2242 ◽  
Author(s):  
Amy Ruddenklau ◽  
Rebecca E Campbell
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Neuronal Network ◽  
Negative Feedback ◽  
Polycystic Ovary ◽  
Steroid Hormone ◽  
Unknown Etiology ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
The Brain

Abstract Polycystic ovary syndrome (PCOS) is a prevalent and distressing disorder of largely unknown etiology. Although PCOS defined by ovarian dysfunction, accumulating evidence supports a critical role for the brain in the ontogeny and pathophysiology of PCOS. A critical pathological feature of PCOS is impaired gonadal steroid hormone negative feedback to the GnRH neuronal network in the brain that regulates fertility. This impairment is associated with androgen excess, a cardinal feature of PCOS. Impaired steroid hormone feedback to GnRH neurons is thought to drive hyperactivity of the neuroendocrine axis controlling fertility, leading to a vicious cycle of androgen excess and reproductive dysfunction. Decades of clinical research have been unable to uncover the mechanisms underlying this impairment, because of the extreme difficulty in studying the brain in humans. It is only recently, with the development of preclinical models of PCOS, that we have begun to unravel the role of the brain in the development and progression of PCOS. Here, we provide a succinct overview of what is known about alterations in the steroid hormone–sensitive GnRH neuronal network that may underlie the neuroendocrine defects in clinical PCOS, with a particular focus on those that may contribute to impaired progesterone negative feedback, and the likely role of androgens in driving this impairment.

scholarly journals Role of Androgen Excess on Metabolic Aberrations and Cardiovascular Risk in Women with Polycystic Ovary Syndrome

2008 ◽  
Vol 4 (6) ◽  
pp. 583-594 ◽  
Author(s):  
Charikleia D Christakou ◽  
Evanthia Diamanti-Kandarakis
Keyword(s):  
Cardiovascular Risk ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Metabolic Abnormalities ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Major Player ◽  
Artery Disease ◽  
Androgen Levels

Polycystic ovary syndrome (PCOS) is associated with a clustering of metabolic and cardiovascular risk factors. Insulin resistance is implicated as the major player in the metabolic abnormalities and contributes to the increased cardiovascular risk associated with the syndrome. However, androgen excess appears to participate as an independent parameter, which further aggravates the cardiovascular and metabolic aberrations in affected women with PCOS. The resultant impact of hyperandrogenemia possibly acquires clinical significance for women's health in the context of PCOS, particularly since recent data support an increased incidence of coronary artery disease and of cardiovascular events directly related to androgen levels in women with the syndrome.

scholarly journals Foetal Sonographic Anogenital Distance Is Longer in Polycystic Ovary Syndrome Mothers

2020 ◽  
Vol 9 (9) ◽  
pp. 2863
Author(s):  
Sharon Perlman ◽  
Yoel Toledano ◽  
Zvi Kivilevitch ◽  
Nufar Halevy ◽  
Elena Rubin ◽  
...  
Keyword(s):  
General Population ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Anogenital Distance ◽  
Appropriate For Gestational Age ◽  
2D Ultrasound ◽  
Diabetic Mothers

Anogenital distance (AGD) is a biomarker for the prenatal hormonal environment. Androgen excess is a key element in polycystic ovary syndrome (PCOS). The aim of this study was to assess the sonographic foetal AGD in a population of PCOS mothers in comparison to the general population. Foetal AGD was measured prospectively by 2D ultrasound in PCOS mothers and compared to prenatal AGD nomograms. The results were interpreted regarding maternal and foetal characteristics. The mean sonographic foetal AGD centile measurement in PCOS mothers was significantly longer in comparison to the general population (86.04% ± 18.22; p < 0.001). Estimated foetal weight and birthweight were appropriate for gestational age and did not correlate with AGD. Sonographic foetal AGD was significantly longer in PCOS diabetic mothers and in those who conceived following assisted reproduction treatments when compared to the general population (p < 0.001). Our results support the role of AGD as a biomarker of the prenatal hormonal environment and provide evidence for the hyperandrogenic effect in PCOS pregnancies on foetal androgenic status and genitalia development.

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