Literature DB >> 28453773

Increased cerebrospinal fluid levels of GABA, testosterone and estradiol in women with polycystic ovary syndrome.

Jennifer F Kawwass1, Kristen M Sanders2, Tammy L Loucks3, Lisa Cencia Rohan4, Sarah L Berga5.   

Abstract

STUDY QUESTION: Do cerebrospinal fluid (CSF) concentrations of gamma-aminobutyric acid (GABA), testosterone (T) and estradiol (E2) differ in women with polycystic ovary syndrome (PCOS) as compared to eumenorrheic, ovulatory women (EW)? SUMMARY ANSWER: Women with PCOS displayed higher CSF levels of GABA and E2, and possibly T, than EW. WHAT IS KNOWN ALREADY: The chronic anovulation characteristic of PCOS has been attributed to increased central GnRH drive and resulting gonadotropin aberrations. Androgens are thought to regulate GABA, which in turn regulates the neural cascade that modulates GnRH drive. STUDY DESIGN, SIZE, DURATION: This cross-sectional observational study included 15 EW and 12 non-obese women with PCOS who consented to a lumbar puncture in addition to 24 h of serum blood collection at 15-min intervals. PARTICIPANTS/MATERIALS, SETTING,
METHODS: In total, 27 women were studied at a the General Clinical Research Center (GCRC) at the University of Pittsburgh. Serum analytes included T, E2 and androstenedione. CSF analytes included GABA, glutamate, glucose, T and E2. MAIN RESULTS AND THE ROLE OF CHANCE: Women with PCOS had higher CSF GABA as compared to EW (9.04 versus 7.04 μmol/L, P < 0.05). CSF glucose and glutamate concentrations were similar between the two groups. CSF T was 52% higher (P = 0.1) and CSF E2 was 30% higher (P < 0.01) in women with PCOS compared to EW. Circulating T was 122% higher (P < 0.01) and circulating E2 was 75% higher (P < 0.01) in women with PCOS than in EW. LIMITATIONS REASONS FOR CAUTION: The study is limited by its small sample size and the technical limitations of measuring CSF analytes that are pulsatile and have short half-lives. WIDER IMPLICATIONS OF THE
FINDINGS: Women with PCOS displayed significantly higher circulating levels of T and E2, significantly higher CSF levels of E2, and higher levels of CSF testosterone, although the latter was not statistically significant. A better understanding of the central milieu informs our understanding of the mechanisms mediating increased the GnRH drive in PCOS and lends a new perspective for understanding the presentation, pathogenesis and potential health consequences of PCOS, including gender identity issues. STUDY FUNDING/COMPETING INTEREST(S): No conflicts of interest. The study was funded by NIH grants to SLB (RO1-MH50748, U54-HD08610) and NIH RR-00056 to the General Clinical Research Center of the University of Pittsburgh. TRIAL REGISTRATION NUMBER: NCT01674426.
© The Author 2017. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com

Entities:  

Keywords:  CSF; GABA; estradiol; polycystic ovary syndrome; testosterone

Mesh:

Substances:

Year:  2017        PMID: 28453773      PMCID: PMC6251519          DOI: 10.1093/humrep/dex086

Source DB:  PubMed          Journal:  Hum Reprod        ISSN: 0268-1161            Impact factor:   6.918


  55 in total

1.  Circulating leptin concentrations in polycystic ovary syndrome: relation to anthropometric and metabolic parameters.

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Journal:  Obstet Gynecol Clin North Am       Date:  2001-03       Impact factor: 2.844

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7.  Increased luteinizing hormone and alpha-subunit secretion in women with hyperandrogenic anovulation.

Authors:  S L Berga; D S Guzick; S J Winters
Journal:  J Clin Endocrinol Metab       Date:  1993-10       Impact factor: 5.958

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9.  Functional neuroimaging of emotional processing in women with polycystic ovary syndrome: a case-control pilot study.

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10.  Ovarian steroids stimulate adenosine triphosphate-sensitive potassium (KATP) channel subunit gene expression and confer responsiveness of the gonadotropin-releasing hormone pulse generator to KATP channel modulation.

Authors:  Wenyu Huang; Maricedes Acosta-Martínez; Jon E Levine
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Review 1.  Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome.

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2.  Prepubertal Development of GABAergic Transmission to Gonadotropin-Releasing Hormone (GnRH) Neurons and Postsynaptic Response Are Altered by Prenatal Androgenization.

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Journal:  J Neurosci       Date:  2018-01-26       Impact factor: 6.167

3.  Ontogeny and reversal of brain circuit abnormalities in a preclinical model of PCOS.

Authors:  Mauro Sb Silva; Melanie Prescott; Rebecca E Campbell
Journal:  JCI Insight       Date:  2018-04-05

Review 4.  The role of gonadotropin-releasing hormone neurons in polycystic ovary syndrome.

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Review 5.  Modulation of Gonadotropin-Releasing Hormone Neuron Activity and Secretion in Mice by Non-peptide Neurotransmitters, Gasotransmitters, and Gliotransmitters.

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6.  A unique androgen excess signature in idiopathic intracranial hypertension is linked to cerebrospinal fluid dynamics.

Authors:  Michael W O'Reilly; Connar Sj Westgate; Catherine Hornby; Hannah Botfield; Angela E Taylor; Keira Markey; James L Mitchell; William J Scotton; Susan P Mollan; Andreas Yiangou; Carl Jenkinson; Lorna C Gilligan; Mark Sherlock; James Gibney; Jeremy W Tomlinson; Gareth G Lavery; David J Hodson; Wiebke Arlt; Alexandra J Sinclair
Journal:  JCI Insight       Date:  2019-03-21

7.  Abnormal GnRH Pulsatility in Polycystic Ovary Syndrome: Recent Insights.

Authors:  Christopher R McCartney; Rebecca E Campbell
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8.  Gut microbiota alterations reveal potential gut-brain axis changes in polycystic ovary syndrome.

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Journal:  J Endocrinol Invest       Date:  2021-01-02       Impact factor: 4.256

Review 9.  Endometriosis and polycystic ovary syndrome are diametric disorders.

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Journal:  Evol Appl       Date:  2021-05-14       Impact factor: 4.929

Review 10.  The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS).

Authors:  Eulalia A Coutinho; Alexander S Kauffman
Journal:  Med Sci (Basel)       Date:  2019-08-02
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