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The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)

Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder, affecting at least 10% of women of reproductive age. PCOS is typically characterized by the presence of at least two of the three cardinal features of hyperandrogenemia (high circulating androgen levels), oligo- or anovula...

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Autores principales: Coutinho, Eulalia A., Kauffman, Alexander S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722593/
https://www.ncbi.nlm.nih.gov/pubmed/31382541
http://dx.doi.org/10.3390/medsci7080084
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author Coutinho, Eulalia A.
Kauffman, Alexander S.
author_facet Coutinho, Eulalia A.
Kauffman, Alexander S.
author_sort Coutinho, Eulalia A.
collection PubMed
description Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder, affecting at least 10% of women of reproductive age. PCOS is typically characterized by the presence of at least two of the three cardinal features of hyperandrogenemia (high circulating androgen levels), oligo- or anovulation, and cystic ovaries. Hyperandrogenemia increases the severity of the condition and is driven by increased luteinizing hormone (LH) pulse secretion from the pituitary. Indeed, PCOS women display both elevated mean LH levels, as well as an elevated frequency of LH pulsatile secretion. The abnormally high LH pulse frequency, reflective of a hyperactive gonadotropin-releasing hormone (GnRH) neural circuit, suggests a neuroendocrine basis to either the etiology or phenotype of PCOS. Several studies in preclinical animal models of PCOS have demonstrated alterations in GnRH neurons and their upstream afferent neuronal circuits. Some rodent PCOS models have demonstrated an increase in GnRH neuron activity that correlates with an increase in stimulatory GABAergic innervation and postsynaptic currents onto GnRH neurons. Additional studies have identified robust increases in hypothalamic levels of kisspeptin, another potent stimulator of GnRH neurons. This review outlines the different brain and neuroendocrine changes in the reproductive axis observed in PCOS animal models, discusses how they might contribute to either the etiology or adult phenotype of PCOS, and considers parallel findings in PCOS women.
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spelling pubmed-67225932019-09-10 The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS) Coutinho, Eulalia A. Kauffman, Alexander S. Med Sci (Basel) Review Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder, affecting at least 10% of women of reproductive age. PCOS is typically characterized by the presence of at least two of the three cardinal features of hyperandrogenemia (high circulating androgen levels), oligo- or anovulation, and cystic ovaries. Hyperandrogenemia increases the severity of the condition and is driven by increased luteinizing hormone (LH) pulse secretion from the pituitary. Indeed, PCOS women display both elevated mean LH levels, as well as an elevated frequency of LH pulsatile secretion. The abnormally high LH pulse frequency, reflective of a hyperactive gonadotropin-releasing hormone (GnRH) neural circuit, suggests a neuroendocrine basis to either the etiology or phenotype of PCOS. Several studies in preclinical animal models of PCOS have demonstrated alterations in GnRH neurons and their upstream afferent neuronal circuits. Some rodent PCOS models have demonstrated an increase in GnRH neuron activity that correlates with an increase in stimulatory GABAergic innervation and postsynaptic currents onto GnRH neurons. Additional studies have identified robust increases in hypothalamic levels of kisspeptin, another potent stimulator of GnRH neurons. This review outlines the different brain and neuroendocrine changes in the reproductive axis observed in PCOS animal models, discusses how they might contribute to either the etiology or adult phenotype of PCOS, and considers parallel findings in PCOS women. MDPI 2019-08-02 /pmc/articles/PMC6722593/ /pubmed/31382541 http://dx.doi.org/10.3390/medsci7080084 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Coutinho, Eulalia A.
Kauffman, Alexander S.
The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)
title The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)
title_full The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)
title_fullStr The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)
title_full_unstemmed The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)
title_short The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)
title_sort role of the brain in the pathogenesis and physiology of polycystic ovary syndrome (pcos)
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722593/
https://www.ncbi.nlm.nih.gov/pubmed/31382541
http://dx.doi.org/10.3390/medsci7080084
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