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Altered Steroid Metabolism and Insulin Signaling in PCOS Endometria: Impact in Tissue Function

Authordc.contributor.authorOróstica Arévalo, María Lorena 
Authordc.contributor.authorRosas Chuñil, Carlos 
Authordc.contributor.authorPlaza Parrochia, Francisca 
Authordc.contributor.authorAstorga Leiva, Isis 
Authordc.contributor.authorGabler Neale, Fernando 
Authordc.contributor.authorGarcía Angulo, Víctor 
Authordc.contributor.authorRomero Osses, Carmen 
Authordc.contributor.authorVega Blanco, María Margarita 
Admission datedc.date.accessioned2017-11-27T19:57:01Z
Available datedc.date.available2017-11-27T19:57:01Z
Publication datedc.date.issued2016
Cita de ítemdc.identifier.citationCurrent Pharmaceutical Desing Vol. 22 Núm. 36 Pág. 5614-5624 (2016)es_ES
Identifierdc.identifier.issn1381-6128
Identifierdc.identifier.other10.2174/1381612822666160810111528
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/145843
Abstractdc.description.abstractBackground: Polycystic Ovary Syndrome (PCOS) is a prevalent endocrine/metabolic disorder characterized by hyperandrogenemia and in most cases, by hyper-insulinemia in addition to obesity. Besides ovarian dysfunction, endometrial physiology is also disrupted since this tissue is highly dependent on the action of steroids; in case of conception cycles, high percentage of abortion is observed. Because of the endocrine/metabolic alterations, PCOS-women present high probability to develop hyperplasia and endometrial cancer, where an imbalance of cell proliferation/apoptosis processes is detected. Additionally, insulin pathway and the endometrial energetic homeostasis are also compromised. Methods: The aim of this review was to report molecular alterations related to insulin-resistance and/or obesity in PCOS-women endometria that could drive to infertility. For this, several methods were employed: immunohistocytochemistry, qPCR, western-blot, glucose-uptake, cell cultures, among others. Results: Diminished levels and activity of several insulin signaling pathway molecules, like IRS-1/AS160/PKC., were detected. Concomitantly, a defect in the synthesis and GLUT4 translocation to cell surface is induced. Oral administration of metformin (insulin sensitizer) to PCOS-patients increases GLUT4 endometrial levels, improving fertility of those patients. Another relevant feature is the high percentage of obesity in PCOS-women; adiponectin is an obesity marker and elicits an insulin-sensitizer action, being diminished in plasma of obese PCOS-women similar to its endometrial level, adiponectin-receptors and APPL1, an adapter molecule of adiponectin pathway. Moreover, obesity and PCOS can induce a pro-inflammatory environment, exaggerating the alterations in insulin pathway. Conclusion: The evidences obtained in PCOS-endometria clearly indicate that these molecular defects could partially explain the reproductive failures of these patientses_ES
Patrocinadordc.description.sponsorshipFONDECYT 1130053 CONICYT 24121153 24121256 21100275 21120541es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherBentham Sciencees_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceCurrent Pharmaceutical Desinges_ES
Keywordsdc.subjectPCOSes_ES
Keywordsdc.subjectEndometriaes_ES
Keywordsdc.subjectInsulines_ES
Keywordsdc.subjectHyperandrogenismes_ES
Keywordsdc.subjectAdiponectines_ES
Keywordsdc.subjectObesityes_ES
Keywordsdc.subjectGlucose-uptakees_ES
Títulodc.titleAltered Steroid Metabolism and Insulin Signaling in PCOS Endometria: Impact in Tissue Functiones_ES
Document typedc.typeArtículo de revistaes_ES
Catalogueruchile.catalogadorapces_ES
Indexationuchile.indexArtículo de publicación ISIes_ES
Access notedct.AccessRightsSin acceso a texto completoes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile