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Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation

As a common endocrinopathy of reproductive-aged women, polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. It is linked with insulin resistance through preferential abdominal fat accumulation that is worsened by obesity. Over th...

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Autores principales: Dumesic, Daniel A., Padmanabhan, Vasantha, Chazenbalk, Gregorio D., Abbott, David H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8744313/
https://www.ncbi.nlm.nih.gov/pubmed/35012577
http://dx.doi.org/10.1186/s12958-021-00878-y
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author Dumesic, Daniel A.
Padmanabhan, Vasantha
Chazenbalk, Gregorio D.
Abbott, David H.
author_facet Dumesic, Daniel A.
Padmanabhan, Vasantha
Chazenbalk, Gregorio D.
Abbott, David H.
author_sort Dumesic, Daniel A.
collection PubMed
description As a common endocrinopathy of reproductive-aged women, polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. It is linked with insulin resistance through preferential abdominal fat accumulation that is worsened by obesity. Over the past two millennia, menstrual irregularity, male-type habitus and sub-infertility have been described in women and confirm that these clinical features of PCOS were common in antiquity. Recent findings in normal-weight hyperandrogenic PCOS women show that exaggerated lipid accumulation by subcutaneous (SC) abdominal stem cells during development to adipocytes in vitro occurs in combination with reduced insulin sensitivity and preferential accumulation of highly-lipolytic intra-abdominal fat in vivo. This PCOS phenotype may be an evolutionary metabolic adaptation to balance energy storage with glucose availability and fatty acid oxidation for optimal energy use during reproduction. This review integrates fundamental endocrine-metabolic changes in healthy, normal-weight PCOS women with similar PCOS-like traits present in animal models in which tissue differentiation is completed during fetal life as in humans to support the evolutionary concept that PCOS has common ancestral and developmental origins.
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spelling pubmed-87443132022-01-11 Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation Dumesic, Daniel A. Padmanabhan, Vasantha Chazenbalk, Gregorio D. Abbott, David H. Reprod Biol Endocrinol Review As a common endocrinopathy of reproductive-aged women, polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. It is linked with insulin resistance through preferential abdominal fat accumulation that is worsened by obesity. Over the past two millennia, menstrual irregularity, male-type habitus and sub-infertility have been described in women and confirm that these clinical features of PCOS were common in antiquity. Recent findings in normal-weight hyperandrogenic PCOS women show that exaggerated lipid accumulation by subcutaneous (SC) abdominal stem cells during development to adipocytes in vitro occurs in combination with reduced insulin sensitivity and preferential accumulation of highly-lipolytic intra-abdominal fat in vivo. This PCOS phenotype may be an evolutionary metabolic adaptation to balance energy storage with glucose availability and fatty acid oxidation for optimal energy use during reproduction. This review integrates fundamental endocrine-metabolic changes in healthy, normal-weight PCOS women with similar PCOS-like traits present in animal models in which tissue differentiation is completed during fetal life as in humans to support the evolutionary concept that PCOS has common ancestral and developmental origins. BioMed Central 2022-01-10 /pmc/articles/PMC8744313/ /pubmed/35012577 http://dx.doi.org/10.1186/s12958-021-00878-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Dumesic, Daniel A.
Padmanabhan, Vasantha
Chazenbalk, Gregorio D.
Abbott, David H.
Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
title Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
title_full Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
title_fullStr Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
title_full_unstemmed Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
title_short Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
title_sort polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8744313/
https://www.ncbi.nlm.nih.gov/pubmed/35012577
http://dx.doi.org/10.1186/s12958-021-00878-y
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