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Insulin and hyperandrogenism in women with polycystic ovary syndrome.
J Steroid Biochem Mol Biol. 2010 Oct; 122(1-3):42-52.JS

Abstract

Polycystic ovary syndrome (PCOS) is a very common endocrine disorder characterized by chronic anovulation, clinical and/or biochemical hyperandrogenism, and/or polycystic ovaries. But most experts consider that hyperandrogenism is the main characteristic of PCOS. Several theories propose different mechanisms to explain PCOS manifestations: (1) a primary enzymatic default in the ovarian and/or adrenal steroidogenesis; (2) an impairment in gonadotropin releasing hormone (GnRH) secretion that promotes luteal hormone (LH) secretion; or (3) alterations in insulin actions that lead to insulin resistance with compensatory hyperinsulinemia. However, in the past 20 years there has been growing evidence supporting that defects in insulin actions or in the insulin signalling pathways are central in the pathogenesis of the syndrome. Indeed, most women with PCOS are metabolically insulin resistant, in part due to genetic predisposition and in part secondary to obesity. But some women with typical PCOS do not display insulin resistance, which supports the hypothesis of a genetic predisposition specific to PCOS that would be revealed by the development of insulin resistance and compensatory hyperinsulinemia in most, but not all, women with PCOS. However, these hypotheses are not yet appropriately confirmed, and more research is still needed to unravel the true pathogenesis underlying this syndrome. The present review thus aims at discussing new concepts and findings regarding insulin actions in PCOS women and how it is related to hyperandrogenemia.

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Authors+Show Affiliations

Baptiste CG
Department of Medicine, Division of Endocrinology, University of Sherbrooke, 3001 12th North Avenue, Sherbrooke, QC J1H 5N4, Canada.
Battista MC
No affiliation info available
Trottier A
No affiliation info available
Baillargeon JP
No affiliation info available

MeSH

FemaleGenetic Predisposition to DiseaseHumansHyperandrogenismHyperinsulinismInsulinInsulin ResistancePolycystic Ovary SyndromeSteroid 17-alpha-HydroxylaseWeight Loss

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

20036327

Clinical Trial Links

Myoinositol for the Treatment of Ovarian and Psychiatric Disorder in Polycystic Ovary Syndrome (PCOS) Patients
Effects of Inositol Alone or Associated With Alpha-lipoic Acid in Polycystic Ovary Syndrome Treatment

Citation

Baptiste, Catherine G., et al. "Insulin and Hyperandrogenism in Women With Polycystic Ovary Syndrome." The Journal of Steroid Biochemistry and Molecular Biology, vol. 122, no. 1-3, 2010, pp. 42-52.
Baptiste CG, Battista MC, Trottier A, et al. Insulin and hyperandrogenism in women with polycystic ovary syndrome. J Steroid Biochem Mol Biol. 2010;122(1-3):42-52.
Baptiste, C. G., Battista, M. C., Trottier, A., & Baillargeon, J. P. (2010). Insulin and hyperandrogenism in women with polycystic ovary syndrome. The Journal of Steroid Biochemistry and Molecular Biology, 122(1-3), 42-52. https://doi.org/10.1016/j.jsbmb.2009.12.010
Baptiste CG, et al. Insulin and Hyperandrogenism in Women With Polycystic Ovary Syndrome. J Steroid Biochem Mol Biol. 2010;122(1-3):42-52. PubMed PMID: 20036327.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Insulin and hyperandrogenism in women with polycystic ovary syndrome. AU - Baptiste,Catherine G, AU - Battista,Marie-Claude, AU - Trottier,Andréanne, AU - Baillargeon,Jean-Patrice, Y1 - 2009/12/28/ PY - 2009/10/02/received PY - 2009/12/15/revised PY - 2009/12/18/accepted PY - 2009/12/29/entrez PY - 2009/12/29/pubmed PY - 2010/10/16/medline SP - 42 EP - 52 JF - The Journal of steroid biochemistry and molecular biology JO - J Steroid Biochem Mol Biol VL - 122 IS - 1-3 N2 - Polycystic ovary syndrome (PCOS) is a very common endocrine disorder characterized by chronic anovulation, clinical and/or biochemical hyperandrogenism, and/or polycystic ovaries. But most experts consider that hyperandrogenism is the main characteristic of PCOS. Several theories propose different mechanisms to explain PCOS manifestations: (1) a primary enzymatic default in the ovarian and/or adrenal steroidogenesis; (2) an impairment in gonadotropin releasing hormone (GnRH) secretion that promotes luteal hormone (LH) secretion; or (3) alterations in insulin actions that lead to insulin resistance with compensatory hyperinsulinemia. However, in the past 20 years there has been growing evidence supporting that defects in insulin actions or in the insulin signalling pathways are central in the pathogenesis of the syndrome. Indeed, most women with PCOS are metabolically insulin resistant, in part due to genetic predisposition and in part secondary to obesity. But some women with typical PCOS do not display insulin resistance, which supports the hypothesis of a genetic predisposition specific to PCOS that would be revealed by the development of insulin resistance and compensatory hyperinsulinemia in most, but not all, women with PCOS. However, these hypotheses are not yet appropriately confirmed, and more research is still needed to unravel the true pathogenesis underlying this syndrome. The present review thus aims at discussing new concepts and findings regarding insulin actions in PCOS women and how it is related to hyperandrogenemia. SN - 1879-1220 UR - https://www.unboundmedicine.com/medline/citation/20036327/Insulin_and_hyperandrogenism_in_women_with_polycystic_ovary_syndrome_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0960-0760(09)00303-3 DB - PRIME DP - Unbound Medicine ER -