Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFLA |
Texto Completo: | http://repositorio.ufla.br/jspui/handle/1/33071 |
Resumo: | This study analyzes whether autonomic dysfunction precedes cardiometabolic alterations in spontaneously hypertensive rats (SHR) with fructose overload. Animals were randomly distributed into three groups: control, hypertensive and hypertensive with fructose overload. Fructose overload (100 g/L) was initiated at 30 days old, and the animals (n = 6/group/time) were evaluated after 7, 15, 30 and 60 days of fructose consumption. Fructose consumption reduced baroreflex sensitivity by day 7, and still induced a progressive reduction in baroreflex sensitivity over the time. Fructose consumption also increased TNFα and IL-6 levels in the adipose tissue and IL-1β levels in the spleen at days 15 and 30. Fructose consumption also reduced plasmatic nitrites (day 15 and 30) and superoxide dismutase activity (day 15 and 60), but increased hydrogen peroxide (day 30 and 60), lipid peroxidation and protein oxidation (day 60). Fructose consumption increased arterial pressure at day 30 (8%) and 60 (11%). Fructose consumption also induced a late insulin resistance at day 60, but did not affect glucose levels. In conclusion, the results show that baroreflex sensitivity impairment precedes inflammatory and oxidative stress disorders, probably by inducing hemodynamic and metabolic dysfunctions observed in metabolic syndrome. |
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Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stressSpontaneously hypertensive ratsBaroreflexMetabolic syndromeRatos espontaneamente hipertensosBarorreflexoSíndrome metabólicaThis study analyzes whether autonomic dysfunction precedes cardiometabolic alterations in spontaneously hypertensive rats (SHR) with fructose overload. Animals were randomly distributed into three groups: control, hypertensive and hypertensive with fructose overload. Fructose overload (100 g/L) was initiated at 30 days old, and the animals (n = 6/group/time) were evaluated after 7, 15, 30 and 60 days of fructose consumption. Fructose consumption reduced baroreflex sensitivity by day 7, and still induced a progressive reduction in baroreflex sensitivity over the time. Fructose consumption also increased TNFα and IL-6 levels in the adipose tissue and IL-1β levels in the spleen at days 15 and 30. Fructose consumption also reduced plasmatic nitrites (day 15 and 30) and superoxide dismutase activity (day 15 and 60), but increased hydrogen peroxide (day 30 and 60), lipid peroxidation and protein oxidation (day 60). Fructose consumption increased arterial pressure at day 30 (8%) and 60 (11%). Fructose consumption also induced a late insulin resistance at day 60, but did not affect glucose levels. In conclusion, the results show that baroreflex sensitivity impairment precedes inflammatory and oxidative stress disorders, probably by inducing hemodynamic and metabolic dysfunctions observed in metabolic syndrome.Nature2019-02-27T10:38:30Z2019-02-27T10:38:30Z2018info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfBERNARDES, N. et al. Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress. Scientific Reports, [S. l.], v. 8, p. 1-10, 2018. doi: 10.1038/s41598-018-26816-4.http://repositorio.ufla.br/jspui/handle/1/33071Scientific Reportsreponame:Repositório Institucional da UFLAinstname:Universidade Federal de Lavras (UFLA)instacron:UFLAhttp://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessBernardes, NathaliaDias, Danielle da SilvaStoyell-Conti, Filipe FernandesBrito-Monzani, Janaina de OliveiraMalfitano, ChristianeCaldini, Elia GarciaUlloa, LuisLlesuy, Susana FranciscaIrigoyen, Maria-CláudiaAngelis, Kátia deeng2023-06-01T10:52:22Zoai:localhost:1/33071Repositório InstitucionalPUBhttp://repositorio.ufla.br/oai/requestnivaldo@ufla.br || repositorio.biblioteca@ufla.bropendoar:2023-06-01T10:52:22Repositório Institucional da UFLA - Universidade Federal de Lavras (UFLA)false |
dc.title.none.fl_str_mv |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress |
title |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress |
spellingShingle |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress Bernardes, Nathalia Spontaneously hypertensive rats Baroreflex Metabolic syndrome Ratos espontaneamente hipertensos Barorreflexo Síndrome metabólica |
title_short |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress |
title_full |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress |
title_fullStr |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress |
title_full_unstemmed |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress |
title_sort |
Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress |
author |
Bernardes, Nathalia |
author_facet |
Bernardes, Nathalia Dias, Danielle da Silva Stoyell-Conti, Filipe Fernandes Brito-Monzani, Janaina de Oliveira Malfitano, Christiane Caldini, Elia Garcia Ulloa, Luis Llesuy, Susana Francisca Irigoyen, Maria-Cláudia Angelis, Kátia de |
author_role |
author |
author2 |
Dias, Danielle da Silva Stoyell-Conti, Filipe Fernandes Brito-Monzani, Janaina de Oliveira Malfitano, Christiane Caldini, Elia Garcia Ulloa, Luis Llesuy, Susana Francisca Irigoyen, Maria-Cláudia Angelis, Kátia de |
author2_role |
author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Bernardes, Nathalia Dias, Danielle da Silva Stoyell-Conti, Filipe Fernandes Brito-Monzani, Janaina de Oliveira Malfitano, Christiane Caldini, Elia Garcia Ulloa, Luis Llesuy, Susana Francisca Irigoyen, Maria-Cláudia Angelis, Kátia de |
dc.subject.por.fl_str_mv |
Spontaneously hypertensive rats Baroreflex Metabolic syndrome Ratos espontaneamente hipertensos Barorreflexo Síndrome metabólica |
topic |
Spontaneously hypertensive rats Baroreflex Metabolic syndrome Ratos espontaneamente hipertensos Barorreflexo Síndrome metabólica |
description |
This study analyzes whether autonomic dysfunction precedes cardiometabolic alterations in spontaneously hypertensive rats (SHR) with fructose overload. Animals were randomly distributed into three groups: control, hypertensive and hypertensive with fructose overload. Fructose overload (100 g/L) was initiated at 30 days old, and the animals (n = 6/group/time) were evaluated after 7, 15, 30 and 60 days of fructose consumption. Fructose consumption reduced baroreflex sensitivity by day 7, and still induced a progressive reduction in baroreflex sensitivity over the time. Fructose consumption also increased TNFα and IL-6 levels in the adipose tissue and IL-1β levels in the spleen at days 15 and 30. Fructose consumption also reduced plasmatic nitrites (day 15 and 30) and superoxide dismutase activity (day 15 and 60), but increased hydrogen peroxide (day 30 and 60), lipid peroxidation and protein oxidation (day 60). Fructose consumption increased arterial pressure at day 30 (8%) and 60 (11%). Fructose consumption also induced a late insulin resistance at day 60, but did not affect glucose levels. In conclusion, the results show that baroreflex sensitivity impairment precedes inflammatory and oxidative stress disorders, probably by inducing hemodynamic and metabolic dysfunctions observed in metabolic syndrome. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018 2019-02-27T10:38:30Z 2019-02-27T10:38:30Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
BERNARDES, N. et al. Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress. Scientific Reports, [S. l.], v. 8, p. 1-10, 2018. doi: 10.1038/s41598-018-26816-4. http://repositorio.ufla.br/jspui/handle/1/33071 |
identifier_str_mv |
BERNARDES, N. et al. Baroreflex impairment precedes cardiometabolic dysfunction in an experimental model of metabolic syndrome: role of inflammation and oxidative stress. Scientific Reports, [S. l.], v. 8, p. 1-10, 2018. doi: 10.1038/s41598-018-26816-4. |
url |
http://repositorio.ufla.br/jspui/handle/1/33071 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.rights.driver.fl_str_mv |
http://creativecommons.org/licenses/by/4.0/ info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by/4.0/ |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Nature |
publisher.none.fl_str_mv |
Nature |
dc.source.none.fl_str_mv |
Scientific Reports reponame:Repositório Institucional da UFLA instname:Universidade Federal de Lavras (UFLA) instacron:UFLA |
instname_str |
Universidade Federal de Lavras (UFLA) |
instacron_str |
UFLA |
institution |
UFLA |
reponame_str |
Repositório Institucional da UFLA |
collection |
Repositório Institucional da UFLA |
repository.name.fl_str_mv |
Repositório Institucional da UFLA - Universidade Federal de Lavras (UFLA) |
repository.mail.fl_str_mv |
nivaldo@ufla.br || repositorio.biblioteca@ufla.br |
_version_ |
1823242152482701312 |