Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents
Autor(a) principal: | |
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Data de Publicação: | 2012 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Clinics |
Texto Completo: | https://www.revistas.usp.br/clinics/article/view/47935 |
Resumo: | OBJECTIVES: The aim of this study was to evaluate cardiovascular autonomic function in a rodent obesity model induced by monosodium glutamate injections during the first seven days of life. METHOD: The animals were assigned to control (control, n = 10) and monosodium glutamate (monosodium glutamate, n = 13) groups. Thirty-three weeks after birth, arterial and venous catheters were implanted for arterial pressure measurements, drug administration, and blood sampling. Baroreflex sensitivity was evaluated according to the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine infusion, respectively. Sympathetic and vagal effects were determined by administering methylatropine and propranolol. RESULTS: Body weight, Lee index, and epididymal white adipose tissue values were higher in the monosodium glutamate group in comparison to the control group. The monosodium glutamate-treated rats displayed insulin resistance, as shown by a reduced glucose/insulin index (-62.5%), an increased area under the curve of total insulin secretion during glucose overload (39.3%), and basal hyperinsulinemia. The mean arterial pressure values were higher in the monosodium glutamate rats, whereas heart rate variability (>;7 times), bradycardic responses (>;4 times), and vagal (~38%) and sympathetic effects (~36%) were reduced as compared to the control group. CONCLUSION: Our results suggest that obesity induced by neonatal monosodium glutamate treatment impairs cardiac autonomic function and most likely contributes to increased arterial pressure and insulin resistance. |
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Clinics |
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Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodentsMonosodium GlutamateObesityInsulin ResistanceArterial PressureAutonomic FunctionOBJECTIVES: The aim of this study was to evaluate cardiovascular autonomic function in a rodent obesity model induced by monosodium glutamate injections during the first seven days of life. METHOD: The animals were assigned to control (control, n = 10) and monosodium glutamate (monosodium glutamate, n = 13) groups. Thirty-three weeks after birth, arterial and venous catheters were implanted for arterial pressure measurements, drug administration, and blood sampling. Baroreflex sensitivity was evaluated according to the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine infusion, respectively. Sympathetic and vagal effects were determined by administering methylatropine and propranolol. RESULTS: Body weight, Lee index, and epididymal white adipose tissue values were higher in the monosodium glutamate group in comparison to the control group. The monosodium glutamate-treated rats displayed insulin resistance, as shown by a reduced glucose/insulin index (-62.5%), an increased area under the curve of total insulin secretion during glucose overload (39.3%), and basal hyperinsulinemia. The mean arterial pressure values were higher in the monosodium glutamate rats, whereas heart rate variability (>;7 times), bradycardic responses (>;4 times), and vagal (~38%) and sympathetic effects (~36%) were reduced as compared to the control group. CONCLUSION: Our results suggest that obesity induced by neonatal monosodium glutamate treatment impairs cardiac autonomic function and most likely contributes to increased arterial pressure and insulin resistance.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2012-10-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/4793510.6061/clinics/2012(10)14Clinics; Vol. 67 No. 10 (2012); 1209-1214Clinics; v. 67 n. 10 (2012); 1209-1214Clinics; Vol. 67 Núm. 10 (2012); 1209-12141980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/47935/51675Konrad, Signorá PeresFarah, VeraRodrigues, BrunoWichi, Rogério BrandãoMachado, Ubiratan FabresLopes, Heno FerreiraSchaan, Beatriz D'AgordAngelis, Kátia DeIrigoyen, Maria Cláudiainfo:eu-repo/semantics/openAccess2012-12-13T11:01:12Zoai:revistas.usp.br:article/47935Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2012-12-13T11:01:12Clinics - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents |
title |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents |
spellingShingle |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents Konrad, Signorá Peres Monosodium Glutamate Obesity Insulin Resistance Arterial Pressure Autonomic Function |
title_short |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents |
title_full |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents |
title_fullStr |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents |
title_full_unstemmed |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents |
title_sort |
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents |
author |
Konrad, Signorá Peres |
author_facet |
Konrad, Signorá Peres Farah, Vera Rodrigues, Bruno Wichi, Rogério Brandão Machado, Ubiratan Fabres Lopes, Heno Ferreira Schaan, Beatriz D'Agord Angelis, Kátia De Irigoyen, Maria Cláudia |
author_role |
author |
author2 |
Farah, Vera Rodrigues, Bruno Wichi, Rogério Brandão Machado, Ubiratan Fabres Lopes, Heno Ferreira Schaan, Beatriz D'Agord Angelis, Kátia De Irigoyen, Maria Cláudia |
author2_role |
author author author author author author author author |
dc.contributor.author.fl_str_mv |
Konrad, Signorá Peres Farah, Vera Rodrigues, Bruno Wichi, Rogério Brandão Machado, Ubiratan Fabres Lopes, Heno Ferreira Schaan, Beatriz D'Agord Angelis, Kátia De Irigoyen, Maria Cláudia |
dc.subject.por.fl_str_mv |
Monosodium Glutamate Obesity Insulin Resistance Arterial Pressure Autonomic Function |
topic |
Monosodium Glutamate Obesity Insulin Resistance Arterial Pressure Autonomic Function |
description |
OBJECTIVES: The aim of this study was to evaluate cardiovascular autonomic function in a rodent obesity model induced by monosodium glutamate injections during the first seven days of life. METHOD: The animals were assigned to control (control, n = 10) and monosodium glutamate (monosodium glutamate, n = 13) groups. Thirty-three weeks after birth, arterial and venous catheters were implanted for arterial pressure measurements, drug administration, and blood sampling. Baroreflex sensitivity was evaluated according to the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine infusion, respectively. Sympathetic and vagal effects were determined by administering methylatropine and propranolol. RESULTS: Body weight, Lee index, and epididymal white adipose tissue values were higher in the monosodium glutamate group in comparison to the control group. The monosodium glutamate-treated rats displayed insulin resistance, as shown by a reduced glucose/insulin index (-62.5%), an increased area under the curve of total insulin secretion during glucose overload (39.3%), and basal hyperinsulinemia. The mean arterial pressure values were higher in the monosodium glutamate rats, whereas heart rate variability (>;7 times), bradycardic responses (>;4 times), and vagal (~38%) and sympathetic effects (~36%) were reduced as compared to the control group. CONCLUSION: Our results suggest that obesity induced by neonatal monosodium glutamate treatment impairs cardiac autonomic function and most likely contributes to increased arterial pressure and insulin resistance. |
publishDate |
2012 |
dc.date.none.fl_str_mv |
2012-10-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://www.revistas.usp.br/clinics/article/view/47935 10.6061/clinics/2012(10)14 |
url |
https://www.revistas.usp.br/clinics/article/view/47935 |
identifier_str_mv |
10.6061/clinics/2012(10)14 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://www.revistas.usp.br/clinics/article/view/47935/51675 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
dc.source.none.fl_str_mv |
Clinics; Vol. 67 No. 10 (2012); 1209-1214 Clinics; v. 67 n. 10 (2012); 1209-1214 Clinics; Vol. 67 Núm. 10 (2012); 1209-1214 1980-5322 1807-5932 reponame:Clinics instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Clinics |
collection |
Clinics |
repository.name.fl_str_mv |
Clinics - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
||clinics@hc.fm.usp.br |
_version_ |
1800222759175847936 |