Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice

Autores
Quiroga, Sofia; Juárez, Yamila R.; Marcone, María Paula; Vidal, María Agustina; Genaro, Ana María; Burgueño, Adriana Laura
Año de publicación
2021
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fil: Quiroga, Sofia. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Quiroga, Sofia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Juárez, Yamila Raquel. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Juárez, Yamila Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Marcone, María Paula. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Marcone, María Paula. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Vidal, María Agustina. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Vidal, María Agustina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Genaro, Ana María. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Genaro, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Burgueño, Adriana Laura. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Burgueño, Adriana Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Abstract: During gestation, stress exposure increases the risk of developing cognitive and physiological alterations in either the long or short term. Among them, metabolic alterations have been described. Adipose tissue is responsible for the secretion of several factors involved in controlling body weight and energy expenditure, the regulation of insulin sensitivity, and the development of inflammation, among others. Moreover, the liver regulates glucose homeostasis and lipid metabolism, playing an essential role in developing insulin resistance. In this work, we analyzed if prenatal stress leads to alterations in metabolism and the relationship between these alterations and gene expression in the adipose tissue and the liver. Prenatal stress-exposed animals developed disturbances in the glucose and insulin response curve, showing in both tests higher glycemia than the control group. However, they did not exhibit increased body weight. At the same time, in the adipose tissue, we observed an increase in mRNA expression of Leptin and Resistin and a decrease in Adiponectin. In the liver, we observed a lower mRNA expression of several genes involved in glucose metabolism and fatty acid oxidation, such as Sirt1, Pgc1α, Pparα, among others. In both tissues, we observed a lower expression of inflammatory genes. These results suggest that prenatal stress exposure produces insulin resistance at both physiological and molecular levels without pro-inflammatory signaling or obesity.
Fuente
Stress: The International Journal on the Biology of Stress Vol.24, No.6, 2021
Materia
ESTRES PRENATAL
EXPRESION GENICA
HIGADO
TEJIDO ADIPOSO
RESISTENCIA A LA INSULINA
PROGRAMACION FETAL
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/14594
Acceder
id RIUCA_be7b0545d1b359becfcae2d5f1ee0961
oai_identifier_str oai:ucacris:123456789/14594
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male miceQuiroga, SofiaJuárez, Yamila R.Marcone, María PaulaVidal, María AgustinaGenaro, Ana MaríaBurgueño, Adriana LauraESTRES PRENATALEXPRESION GENICAHIGADOTEJIDO ADIPOSORESISTENCIA A LA INSULINAPROGRAMACION FETALFil: Quiroga, Sofia. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Quiroga, Sofia. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Juárez, Yamila Raquel. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Juárez, Yamila Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Marcone, María Paula. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Marcone, María Paula. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Vidal, María Agustina. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Vidal, María Agustina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Genaro, Ana María. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Genaro, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Burgueño, Adriana Laura. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Burgueño, Adriana Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaAbstract: During gestation, stress exposure increases the risk of developing cognitive and physiological alterations in either the long or short term. Among them, metabolic alterations have been described. Adipose tissue is responsible for the secretion of several factors involved in controlling body weight and energy expenditure, the regulation of insulin sensitivity, and the development of inflammation, among others. Moreover, the liver regulates glucose homeostasis and lipid metabolism, playing an essential role in developing insulin resistance. In this work, we analyzed if prenatal stress leads to alterations in metabolism and the relationship between these alterations and gene expression in the adipose tissue and the liver. Prenatal stress-exposed animals developed disturbances in the glucose and insulin response curve, showing in both tests higher glycemia than the control group. However, they did not exhibit increased body weight. At the same time, in the adipose tissue, we observed an increase in mRNA expression of Leptin and Resistin and a decrease in Adiponectin. In the liver, we observed a lower mRNA expression of several genes involved in glucose metabolism and fatty acid oxidation, such as Sirt1, Pgc1α, Pparα, among others. In both tissues, we observed a lower expression of inflammatory genes. These results suggest that prenatal stress exposure produces insulin resistance at both physiological and molecular levels without pro-inflammatory signaling or obesity.Taylor & Francis2021info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/1459410.1080/10253890.2021.197842534581257Quiroga, S. et al. Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice [en línea]. Stress: The International Journal on the Biology of Stress. 2021, 24 (6). doi: 10.1080/10253890.2021.1978425. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14594Stress: The International Journal on the Biology of Stress Vol.24, No.6, 2021reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:58:43Zoai:ucacris:123456789/14594instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:58:43.758Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
title Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
spellingShingle Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
Quiroga, Sofia
ESTRES PRENATAL
EXPRESION GENICA
HIGADO
TEJIDO ADIPOSO
RESISTENCIA A LA INSULINA
PROGRAMACION FETAL
title_short Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
title_full Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
title_fullStr Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
title_full_unstemmed Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
title_sort Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
dc.creator.none.fl_str_mv Quiroga, Sofia
Juárez, Yamila R.
Marcone, María Paula
Vidal, María Agustina
Genaro, Ana María
Burgueño, Adriana Laura
author Quiroga, Sofia
author_facet Quiroga, Sofia
Juárez, Yamila R.
Marcone, María Paula
Vidal, María Agustina
Genaro, Ana María
Burgueño, Adriana Laura
author_role author
author2 Juárez, Yamila R.
Marcone, María Paula
Vidal, María Agustina
Genaro, Ana María
Burgueño, Adriana Laura
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv ESTRES PRENATAL
EXPRESION GENICA
HIGADO
TEJIDO ADIPOSO
RESISTENCIA A LA INSULINA
PROGRAMACION FETAL
topic ESTRES PRENATAL
EXPRESION GENICA
HIGADO
TEJIDO ADIPOSO
RESISTENCIA A LA INSULINA
PROGRAMACION FETAL
dc.description.none.fl_txt_mv Fil: Quiroga, Sofia. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Quiroga, Sofia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Juárez, Yamila Raquel. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Juárez, Yamila Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Marcone, María Paula. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Marcone, María Paula. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Vidal, María Agustina. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Vidal, María Agustina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Genaro, Ana María. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Genaro, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Burgueño, Adriana Laura. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Burgueño, Adriana Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Abstract: During gestation, stress exposure increases the risk of developing cognitive and physiological alterations in either the long or short term. Among them, metabolic alterations have been described. Adipose tissue is responsible for the secretion of several factors involved in controlling body weight and energy expenditure, the regulation of insulin sensitivity, and the development of inflammation, among others. Moreover, the liver regulates glucose homeostasis and lipid metabolism, playing an essential role in developing insulin resistance. In this work, we analyzed if prenatal stress leads to alterations in metabolism and the relationship between these alterations and gene expression in the adipose tissue and the liver. Prenatal stress-exposed animals developed disturbances in the glucose and insulin response curve, showing in both tests higher glycemia than the control group. However, they did not exhibit increased body weight. At the same time, in the adipose tissue, we observed an increase in mRNA expression of Leptin and Resistin and a decrease in Adiponectin. In the liver, we observed a lower mRNA expression of several genes involved in glucose metabolism and fatty acid oxidation, such as Sirt1, Pgc1α, Pparα, among others. In both tissues, we observed a lower expression of inflammatory genes. These results suggest that prenatal stress exposure produces insulin resistance at both physiological and molecular levels without pro-inflammatory signaling or obesity.
description Fil: Quiroga, Sofia. Pontificia Universidad Católica Argentina. Instituto de Investigaciones Biomédicas; Argentina
publishDate 2021
dc.date.none.fl_str_mv 2021
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 https://repositorio.uca.edu.ar/handle/123456789/14594
10.1080/10253890.2021.1978425
34581257
Quiroga, S. et al. Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice [en línea]. Stress: The International Journal on the Biology of Stress. 2021, 24 (6). doi: 10.1080/10253890.2021.1978425. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14594
url https://repositorio.uca.edu.ar/handle/123456789/14594
identifier_str_mv 10.1080/10253890.2021.1978425
34581257
Quiroga, S. et al. Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice [en línea]. Stress: The International Journal on the Biology of Stress. 2021, 24 (6). doi: 10.1080/10253890.2021.1978425. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14594
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Taylor & Francis
publisher.none.fl_str_mv Taylor & Francis
dc.source.none.fl_str_mv Stress: The International Journal on the Biology of Stress Vol.24, No.6, 2021
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
_version_ 1836638363566735360
score 13.13397

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