Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats

Autores
Ferreira, Silvana Rocio; Goyeneche, Alicia Alejandra; Heber, María Florencia; Abruzzese, Giselle Adriana; Ferrer, María José; Telleria, Carlos Marcelo; Motta, Alicia Beatriz
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Prenatal androgen excess is considered one of the main causes of the development of polycystic ovary syndrome. In this study, we investigated the effect of prenatal hyperandrogenization (PH) on the physiology of the adult uterine tissue using a murine model of fetal programming caused by androgen excess in adult female rats. Pregnant rats were hyperandrogenized with testosterone and female offspring were studied when adult. Our results showed that PH leads to hyperglycemia and hyperinsulinemia. Consequently, PH developed insulin resistance and a systemic inflammatory state reflected by increased C-reactive protein. In the uterine tissue, levels of PPAR gamma—an important metabolic sensor in the endometrium—were found to be impaired. Moreover, PH induced a pro-inflammatory and an unbalanced oxidative state in the uterus reflected by increased COX-2, lipid peroxidation, and NF-κB. In summary, our results revealed that PH leads to a compromised metabolic state likely consequence of fetal reprogramming.
Fil: Ferreira, Silvana Rocio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Goyeneche, Alicia Alejandra. McGill University; Canadá
Fil: Heber, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Abruzzese, Giselle Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Ferrer, María José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Telleria, Carlos Marcelo. McGill University; Canadá
Fil: Motta, Alicia Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Materia
FETAL PROGRAMMING
INFLAMMATION
OXIDATIVE STRESS
PRENATAL HYPERANDROGENIZATION
UTERUS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/133017
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/133017
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in ratsFerreira, Silvana RocioGoyeneche, Alicia AlejandraHeber, María FlorenciaAbruzzese, Giselle AdrianaFerrer, María JoséTelleria, Carlos MarceloMotta, Alicia BeatrizFETAL PROGRAMMINGINFLAMMATIONOXIDATIVE STRESSPRENATAL HYPERANDROGENIZATIONUTERUShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Prenatal androgen excess is considered one of the main causes of the development of polycystic ovary syndrome. In this study, we investigated the effect of prenatal hyperandrogenization (PH) on the physiology of the adult uterine tissue using a murine model of fetal programming caused by androgen excess in adult female rats. Pregnant rats were hyperandrogenized with testosterone and female offspring were studied when adult. Our results showed that PH leads to hyperglycemia and hyperinsulinemia. Consequently, PH developed insulin resistance and a systemic inflammatory state reflected by increased C-reactive protein. In the uterine tissue, levels of PPAR gamma—an important metabolic sensor in the endometrium—were found to be impaired. Moreover, PH induced a pro-inflammatory and an unbalanced oxidative state in the uterus reflected by increased COX-2, lipid peroxidation, and NF-κB. In summary, our results revealed that PH leads to a compromised metabolic state likely consequence of fetal reprogramming.Fil: Ferreira, Silvana Rocio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Goyeneche, Alicia Alejandra. McGill University; CanadáFil: Heber, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Abruzzese, Giselle Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Ferrer, María José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Telleria, Carlos Marcelo. McGill University; CanadáFil: Motta, Alicia Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaElsevier Ireland2020-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/133017Ferreira, Silvana Rocio; Goyeneche, Alicia Alejandra; Heber, María Florencia; Abruzzese, Giselle Adriana; Ferrer, María José; et al.; Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats; Elsevier Ireland; Molecular and Cellular Endocrinology; 519; 1-2020; 1-290303-7207CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S0303720720303476info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mce.2020.111045info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:43:49Zoai:ri.conicet.gov.ar:11336/133017instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:43:49.58CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
title Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
spellingShingle Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
Ferreira, Silvana Rocio
FETAL PROGRAMMING
INFLAMMATION
OXIDATIVE STRESS
PRENATAL HYPERANDROGENIZATION
UTERUS
title_short Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
title_full Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
title_fullStr Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
title_full_unstemmed Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
title_sort Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
dc.creator.none.fl_str_mv Ferreira, Silvana Rocio
Goyeneche, Alicia Alejandra
Heber, María Florencia
Abruzzese, Giselle Adriana
Ferrer, María José
Telleria, Carlos Marcelo
Motta, Alicia Beatriz
author Ferreira, Silvana Rocio
author_facet Ferreira, Silvana Rocio
Goyeneche, Alicia Alejandra
Heber, María Florencia
Abruzzese, Giselle Adriana
Ferrer, María José
Telleria, Carlos Marcelo
Motta, Alicia Beatriz
author_role author
author2 Goyeneche, Alicia Alejandra
Heber, María Florencia
Abruzzese, Giselle Adriana
Ferrer, María José
Telleria, Carlos Marcelo
Motta, Alicia Beatriz
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv FETAL PROGRAMMING
INFLAMMATION
OXIDATIVE STRESS
PRENATAL HYPERANDROGENIZATION
UTERUS
topic FETAL PROGRAMMING
INFLAMMATION
OXIDATIVE STRESS
PRENATAL HYPERANDROGENIZATION
UTERUS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Prenatal androgen excess is considered one of the main causes of the development of polycystic ovary syndrome. In this study, we investigated the effect of prenatal hyperandrogenization (PH) on the physiology of the adult uterine tissue using a murine model of fetal programming caused by androgen excess in adult female rats. Pregnant rats were hyperandrogenized with testosterone and female offspring were studied when adult. Our results showed that PH leads to hyperglycemia and hyperinsulinemia. Consequently, PH developed insulin resistance and a systemic inflammatory state reflected by increased C-reactive protein. In the uterine tissue, levels of PPAR gamma—an important metabolic sensor in the endometrium—were found to be impaired. Moreover, PH induced a pro-inflammatory and an unbalanced oxidative state in the uterus reflected by increased COX-2, lipid peroxidation, and NF-κB. In summary, our results revealed that PH leads to a compromised metabolic state likely consequence of fetal reprogramming.
Fil: Ferreira, Silvana Rocio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Goyeneche, Alicia Alejandra. McGill University; Canadá
Fil: Heber, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Abruzzese, Giselle Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Ferrer, María José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Telleria, Carlos Marcelo. McGill University; Canadá
Fil: Motta, Alicia Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
description Prenatal androgen excess is considered one of the main causes of the development of polycystic ovary syndrome. In this study, we investigated the effect of prenatal hyperandrogenization (PH) on the physiology of the adult uterine tissue using a murine model of fetal programming caused by androgen excess in adult female rats. Pregnant rats were hyperandrogenized with testosterone and female offspring were studied when adult. Our results showed that PH leads to hyperglycemia and hyperinsulinemia. Consequently, PH developed insulin resistance and a systemic inflammatory state reflected by increased C-reactive protein. In the uterine tissue, levels of PPAR gamma—an important metabolic sensor in the endometrium—were found to be impaired. Moreover, PH induced a pro-inflammatory and an unbalanced oxidative state in the uterus reflected by increased COX-2, lipid peroxidation, and NF-κB. In summary, our results revealed that PH leads to a compromised metabolic state likely consequence of fetal reprogramming.
publishDate 2020
dc.date.none.fl_str_mv 2020-01
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/133017
Ferreira, Silvana Rocio; Goyeneche, Alicia Alejandra; Heber, María Florencia; Abruzzese, Giselle Adriana; Ferrer, María José; et al.; Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats; Elsevier Ireland; Molecular and Cellular Endocrinology; 519; 1-2020; 1-29
0303-7207
CONICET Digital
CONICET
url http://hdl.handle.net/11336/133017
identifier_str_mv Ferreira, Silvana Rocio; Goyeneche, Alicia Alejandra; Heber, María Florencia; Abruzzese, Giselle Adriana; Ferrer, María José; et al.; Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats; Elsevier Ireland; Molecular and Cellular Endocrinology; 519; 1-2020; 1-29
0303-7207
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S0303720720303476
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mce.2020.111045
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Ireland
publisher.none.fl_str_mv Elsevier Ireland
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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