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Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies.
Mol Metab. 2020 05; 35:100937.MM

Abstract

BACKGROUND

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy among reproductive age women. Although its cardinal manifestations include hyperandrogenism, oligo/anovulation, and/or polycystic ovarian morphology, PCOS women often display also notable metabolic comorbidities. An array of pathogenic mechanisms have been implicated in the etiology of this heterogeneous endocrine disorder; hyperandrogenism at various developmental periods is proposed as a major driver of the metabolic and reproductive perturbations associated with PCOS. However, the current understanding of the pathophysiology of PCOS-associated metabolic disease is incomplete, and therapeutic strategies used to manage this syndrome's metabolic complications remain limited.

SCOPE OF REVIEW

This study is a systematic review of the potential etiopathogenic mechanisms of metabolic dysfunction frequently associated with PCOS, with special emphasis on the metabolic impact of androgen excess on different metabolic tissues and the brain. We also briefly summarize the therapeutic approaches currently available to manage metabolic perturbations linked to PCOS, highlighting current weaknesses and future directions.

MAJOR CONCLUSIONS

Androgen excess plays a prominent role in the development of metabolic disturbances associated with PCOS, with a discernible impact on key peripheral metabolic tissues, including the adipose, liver, pancreas, and muscle, and very prominently the brain, contributing to the constellation of metabolic complications of PCOS, from obesity to insulin resistance. However, the current understanding of the pathogenic roles of hyperandrogenism in metabolic dysfunction of PCOS and the underlying mechanisms remain largely incomplete. In addition, the development of more efficient, even personalized therapeutic strategies for the metabolic management of PCOS patients persists as an unmet need that will certainly benefit from a better comprehension of the molecular basis of this heterogeneous syndrome.

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Authors+Show Affiliations

Sanchez-Garrido MA
Instituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Spain; Department of Cell Biology, Physiology, and Immunology, University of Cordoba, Spain; Hospital Universitario Reina Sofia, Cordoba, Spain; CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III Cordoba, Spain. Electronic address: b12sanom@uco.es.
Tena-Sempere M
Instituto Maimónides de Investigación Biomédica de Cordoba (IMIBIC), Spain; Department of Cell Biology, Physiology, and Immunology, University of Cordoba, Spain; Hospital Universitario Reina Sofia, Cordoba, Spain; CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III Cordoba, Spain; FiDiPro Program, Institute of Biomedicine, University of Turku, FIN-20520 Turku, Finland.

MeSH

Adipose TissueAndrogensAnimalsBariatric SurgeryFemaleHumansHyperandrogenismInsulin ResistanceMetabolic SyndromeMiceObesityPolycystic Ovary Syndrome

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Systematic Review

Language

eng

PubMed ID

32244180

Citation

Sanchez-Garrido, Miguel A., and Manuel Tena-Sempere. "Metabolic Dysfunction in Polycystic Ovary Syndrome: Pathogenic Role of Androgen Excess and Potential Therapeutic Strategies." Molecular Metabolism, vol. 35, 2020, p. 100937.
Sanchez-Garrido MA, Tena-Sempere M. Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies. Mol Metab. 2020;35:100937.
Sanchez-Garrido, M. A., & Tena-Sempere, M. (2020). Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies. Molecular Metabolism, 35, 100937. https://doi.org/10.1016/j.molmet.2020.01.001
Sanchez-Garrido MA, Tena-Sempere M. Metabolic Dysfunction in Polycystic Ovary Syndrome: Pathogenic Role of Androgen Excess and Potential Therapeutic Strategies. Mol Metab. 2020;35:100937. PubMed PMID: 32244180.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies. AU - Sanchez-Garrido,Miguel A, AU - Tena-Sempere,Manuel, Y1 - 2020/02/05/ PY - 2019/11/18/received PY - 2019/12/30/revised PY - 2020/01/03/accepted PY - 2020/4/4/pubmed PY - 2021/4/15/medline PY - 2020/4/4/entrez KW - Androgen excess KW - GLP-1 KW - Insulin resistance KW - Obesity KW - PCOS KW - Poly-agonists SP - 100937 EP - 100937 JF - Molecular metabolism JO - Mol Metab VL - 35 N2 - BACKGROUND: Polycystic ovary syndrome (PCOS) is the most common endocrinopathy among reproductive age women. Although its cardinal manifestations include hyperandrogenism, oligo/anovulation, and/or polycystic ovarian morphology, PCOS women often display also notable metabolic comorbidities. An array of pathogenic mechanisms have been implicated in the etiology of this heterogeneous endocrine disorder; hyperandrogenism at various developmental periods is proposed as a major driver of the metabolic and reproductive perturbations associated with PCOS. However, the current understanding of the pathophysiology of PCOS-associated metabolic disease is incomplete, and therapeutic strategies used to manage this syndrome's metabolic complications remain limited. SCOPE OF REVIEW: This study is a systematic review of the potential etiopathogenic mechanisms of metabolic dysfunction frequently associated with PCOS, with special emphasis on the metabolic impact of androgen excess on different metabolic tissues and the brain. We also briefly summarize the therapeutic approaches currently available to manage metabolic perturbations linked to PCOS, highlighting current weaknesses and future directions. MAJOR CONCLUSIONS: Androgen excess plays a prominent role in the development of metabolic disturbances associated with PCOS, with a discernible impact on key peripheral metabolic tissues, including the adipose, liver, pancreas, and muscle, and very prominently the brain, contributing to the constellation of metabolic complications of PCOS, from obesity to insulin resistance. However, the current understanding of the pathogenic roles of hyperandrogenism in metabolic dysfunction of PCOS and the underlying mechanisms remain largely incomplete. In addition, the development of more efficient, even personalized therapeutic strategies for the metabolic management of PCOS patients persists as an unmet need that will certainly benefit from a better comprehension of the molecular basis of this heterogeneous syndrome. SN - 2212-8778 UR - https://www.unboundmedicine.com/medline/citation/32244180/Metabolic_dysfunction_in_polycystic_ovary_syndrome:_Pathogenic_role_of_androgen_excess_and_potential_therapeutic_strategies_ DB - PRIME DP - Unbound Medicine ER -