Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction
- Autores
- Villagarcía, Hernán Gonzalo; Sabugo, Vanesa; Castro, María Cecilia; Schinella, Guillermo Raúl; Castrogiovanni, Daniel; Spinedi, Eduardo; Massa, María Laura; Francini, Flavio
- Año de publicación
- 2016
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- We investigated the impact of chronic hypercorticosteronemia (due to neonatal monosodium L-glutamate, MSG, and treatment) on liver oxidative stress (OS), inflammation, and carbohydrate/lipid metabolism in adult male rats. We evaluated the peripheral concentrations of several metabolic and OS markers and insulin resistance indexes. In liver we assessed (a) OS (GSH and protein carbonyl groups) and inflammatory (IL-1b, TNFa, and PAI-1) biomarkers and (b) carbohydrate and lipid metabolisms. MSG rats displayed degenerated optic nerves, hypophagia, low body and liver weights, and enlarged adipose tissue mass; higher peripheral levels of glucose, triglycerides, insulin, uric acid, leptin, corticosterone, transaminases and TBARS, and peripheral and liver insulin resistance; elevated liver OS, inflammation markers, and glucokinase (mRNA/activity) and fructokinase (mRNA). Additionally, MSG liver phosphofructokinase-2, glucose-6-phosphatase (mRNA and activity) and glucose-6-phosphate dehydrogenase, Chrebp, Srebp1c, fatty acid synthase, and glycerol-3-phosphate (mRNAs)were increased. In conclusion adultMSGrats developed an insulinresistant state and increased OS and serious hepatic dysfunction characterized by inflammation and metabolic signs suggesting increased lipogenesis.These features, shared by both metabolic and Cushing’s syndrome human phenotypes, support that a chronic glucocorticoid-rich endogenous environment mainly impacts on hepatic glucose cycle, displacing local metabolism to lipogenesis. Whether correcting the glucocorticoid-rich environment ameliorates such dysfunctions requires further investigation.
- Materia
-
Ciencias Químicas
hipercorticosteronemia crónica
estrés oxidativo hepático - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
- OAI Identificador
- oai:digital.cic.gba.gob.ar:11746/7017
Ver los metadatos del registro completo
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Chronic Glucocorticoid-Rich Milieu and Liver DysfunctionVillagarcía, Hernán GonzaloSabugo, VanesaCastro, María CeciliaSchinella, Guillermo RaúlCastrogiovanni, DanielSpinedi, EduardoMassa, María LauraFrancini, FlavioCiencias Químicashipercorticosteronemia crónicaestrés oxidativo hepáticoWe investigated the impact of chronic hypercorticosteronemia (due to neonatal monosodium L-glutamate, MSG, and treatment) on liver oxidative stress (OS), inflammation, and carbohydrate/lipid metabolism in adult male rats. We evaluated the peripheral concentrations of several metabolic and OS markers and insulin resistance indexes. In liver we assessed (a) OS (GSH and protein carbonyl groups) and inflammatory (IL-1b, TNFa, and PAI-1) biomarkers and (b) carbohydrate and lipid metabolisms. MSG rats displayed degenerated optic nerves, hypophagia, low body and liver weights, and enlarged adipose tissue mass; higher peripheral levels of glucose, triglycerides, insulin, uric acid, leptin, corticosterone, transaminases and TBARS, and peripheral and liver insulin resistance; elevated liver OS, inflammation markers, and glucokinase (mRNA/activity) and fructokinase (mRNA). Additionally, MSG liver phosphofructokinase-2, glucose-6-phosphatase (mRNA and activity) and glucose-6-phosphate dehydrogenase, Chrebp, Srebp1c, fatty acid synthase, and glycerol-3-phosphate (mRNAs)were increased. In conclusion adultMSGrats developed an insulinresistant state and increased OS and serious hepatic dysfunction characterized by inflammation and metabolic signs suggesting increased lipogenesis.These features, shared by both metabolic and Cushing’s syndrome human phenotypes, support that a chronic glucocorticoid-rich endogenous environment mainly impacts on hepatic glucose cycle, displacing local metabolism to lipogenesis. Whether correcting the glucocorticoid-rich environment ameliorates such dysfunctions requires further investigation.2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://digital.cic.gba.gob.ar/handle/11746/7017enginfo:eu-repo/semantics/altIdentifier/doi/10.1155/2016/7838290info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/reponame:CIC Digital (CICBA)instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Airesinstacron:CICBA2025-09-29T13:40:15Zoai:digital.cic.gba.gob.ar:11746/7017Institucionalhttp://digital.cic.gba.gob.arOrganismo científico-tecnológicoNo correspondehttp://digital.cic.gba.gob.ar/oai/snrdmarisa.degiusti@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:94412025-09-29 13:40:15.831CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Airesfalse |
dc.title.none.fl_str_mv |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction |
title |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction |
spellingShingle |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction Villagarcía, Hernán Gonzalo Ciencias Químicas hipercorticosteronemia crónica estrés oxidativo hepático |
title_short |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction |
title_full |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction |
title_fullStr |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction |
title_full_unstemmed |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction |
title_sort |
Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction |
dc.creator.none.fl_str_mv |
Villagarcía, Hernán Gonzalo Sabugo, Vanesa Castro, María Cecilia Schinella, Guillermo Raúl Castrogiovanni, Daniel Spinedi, Eduardo Massa, María Laura Francini, Flavio |
author |
Villagarcía, Hernán Gonzalo |
author_facet |
Villagarcía, Hernán Gonzalo Sabugo, Vanesa Castro, María Cecilia Schinella, Guillermo Raúl Castrogiovanni, Daniel Spinedi, Eduardo Massa, María Laura Francini, Flavio |
author_role |
author |
author2 |
Sabugo, Vanesa Castro, María Cecilia Schinella, Guillermo Raúl Castrogiovanni, Daniel Spinedi, Eduardo Massa, María Laura Francini, Flavio |
author2_role |
author author author author author author author |
dc.subject.none.fl_str_mv |
Ciencias Químicas hipercorticosteronemia crónica estrés oxidativo hepático |
topic |
Ciencias Químicas hipercorticosteronemia crónica estrés oxidativo hepático |
dc.description.none.fl_txt_mv |
We investigated the impact of chronic hypercorticosteronemia (due to neonatal monosodium L-glutamate, MSG, and treatment) on liver oxidative stress (OS), inflammation, and carbohydrate/lipid metabolism in adult male rats. We evaluated the peripheral concentrations of several metabolic and OS markers and insulin resistance indexes. In liver we assessed (a) OS (GSH and protein carbonyl groups) and inflammatory (IL-1b, TNFa, and PAI-1) biomarkers and (b) carbohydrate and lipid metabolisms. MSG rats displayed degenerated optic nerves, hypophagia, low body and liver weights, and enlarged adipose tissue mass; higher peripheral levels of glucose, triglycerides, insulin, uric acid, leptin, corticosterone, transaminases and TBARS, and peripheral and liver insulin resistance; elevated liver OS, inflammation markers, and glucokinase (mRNA/activity) and fructokinase (mRNA). Additionally, MSG liver phosphofructokinase-2, glucose-6-phosphatase (mRNA and activity) and glucose-6-phosphate dehydrogenase, Chrebp, Srebp1c, fatty acid synthase, and glycerol-3-phosphate (mRNAs)were increased. In conclusion adultMSGrats developed an insulinresistant state and increased OS and serious hepatic dysfunction characterized by inflammation and metabolic signs suggesting increased lipogenesis.These features, shared by both metabolic and Cushing’s syndrome human phenotypes, support that a chronic glucocorticoid-rich endogenous environment mainly impacts on hepatic glucose cycle, displacing local metabolism to lipogenesis. Whether correcting the glucocorticoid-rich environment ameliorates such dysfunctions requires further investigation. |
description |
We investigated the impact of chronic hypercorticosteronemia (due to neonatal monosodium L-glutamate, MSG, and treatment) on liver oxidative stress (OS), inflammation, and carbohydrate/lipid metabolism in adult male rats. We evaluated the peripheral concentrations of several metabolic and OS markers and insulin resistance indexes. In liver we assessed (a) OS (GSH and protein carbonyl groups) and inflammatory (IL-1b, TNFa, and PAI-1) biomarkers and (b) carbohydrate and lipid metabolisms. MSG rats displayed degenerated optic nerves, hypophagia, low body and liver weights, and enlarged adipose tissue mass; higher peripheral levels of glucose, triglycerides, insulin, uric acid, leptin, corticosterone, transaminases and TBARS, and peripheral and liver insulin resistance; elevated liver OS, inflammation markers, and glucokinase (mRNA/activity) and fructokinase (mRNA). Additionally, MSG liver phosphofructokinase-2, glucose-6-phosphatase (mRNA and activity) and glucose-6-phosphate dehydrogenase, Chrebp, Srebp1c, fatty acid synthase, and glycerol-3-phosphate (mRNAs)were increased. In conclusion adultMSGrats developed an insulinresistant state and increased OS and serious hepatic dysfunction characterized by inflammation and metabolic signs suggesting increased lipogenesis.These features, shared by both metabolic and Cushing’s syndrome human phenotypes, support that a chronic glucocorticoid-rich endogenous environment mainly impacts on hepatic glucose cycle, displacing local metabolism to lipogenesis. Whether correcting the glucocorticoid-rich environment ameliorates such dysfunctions requires further investigation. |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016 |
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://digital.cic.gba.gob.ar/handle/11746/7017 |
url |
https://digital.cic.gba.gob.ar/handle/11746/7017 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1155/2016/7838290 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by/4.0/ |
dc.format.none.fl_str_mv |
application/pdf |
dc.source.none.fl_str_mv |
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CIC Digital (CICBA) |
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Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
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CICBA |
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CICBA |
repository.name.fl_str_mv |
CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
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marisa.degiusti@sedici.unlp.edu.ar |
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