Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice
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.
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Taylor & Francis
2021
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Subjects: | ESTRES PRENATAL, EXPRESION GENICA, HIGADO, TEJIDO ADIPOSO, RESISTENCIA A LA INSULINA, PROGRAMACION FETAL, |
Online Access: | https://repositorio.uca.edu.ar/handle/123456789/14594 |
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oai:ucacris:123456789-145942024-03-26T10:59:09Z Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice Quiroga, Sofia Juárez, Yamila R. Marcone, María Paula Vidal, María Agustina Genaro, Ana María Burgueño, Adriana Laura ESTRES PRENATAL EXPRESION GENICA HIGADO TEJIDO ADIPOSO RESISTENCIA A LA INSULINA PROGRAMACION FETAL 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. 2022-08-02T13:11:18Z 2022-08-02T13:11:18Z 2021 Artículo 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 https://repositorio.uca.edu.ar/handle/123456789/14594 10.1080/10253890.2021.1978425 34581257 eng Acceso abierto http://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf Taylor & Francis Stress: The International Journal on the Biology of Stress Vol.24, No.6, 2021 |
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ESTRES PRENATAL EXPRESION GENICA HIGADO TEJIDO ADIPOSO RESISTENCIA A LA INSULINA PROGRAMACION FETAL ESTRES PRENATAL EXPRESION GENICA HIGADO TEJIDO ADIPOSO RESISTENCIA A LA INSULINA PROGRAMACION FETAL |
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ESTRES PRENATAL EXPRESION GENICA HIGADO TEJIDO ADIPOSO RESISTENCIA A LA INSULINA PROGRAMACION FETAL ESTRES PRENATAL EXPRESION GENICA HIGADO TEJIDO ADIPOSO RESISTENCIA A LA INSULINA PROGRAMACION FETAL Quiroga, Sofia Juárez, Yamila R. Marcone, María Paula Vidal, María Agustina Genaro, Ana María Burgueño, Adriana Laura Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice |
description |
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. |
format |
Artículo |
topic_facet |
ESTRES PRENATAL EXPRESION GENICA HIGADO TEJIDO ADIPOSO RESISTENCIA A LA INSULINA PROGRAMACION FETAL |
author |
Quiroga, Sofia Juárez, Yamila R. Marcone, María Paula Vidal, María Agustina Genaro, Ana María Burgueño, Adriana Laura |
author_facet |
Quiroga, Sofia Juárez, Yamila R. Marcone, María Paula Vidal, María Agustina Genaro, Ana María Burgueño, Adriana Laura |
author_sort |
Quiroga, Sofia |
title |
Prenatal stress promotes insulin resistance without inflammation or obesity in C57BL/6J male mice |
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 |
publisher |
Taylor & Francis |
publishDate |
2021 |
url |
https://repositorio.uca.edu.ar/handle/123456789/14594 |
work_keys_str_mv |
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