Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid

Detalhes bibliográficos
Autor(a) principal: Boschero, Antonio Carlos, 1943-
Data de Publicação: 2014
Tipo de documento: Artigo
Título da fonte: Repositório da Produção Científica e Intelectual da Unicamp
Texto Completo: https://hdl.handle.net/20.500.12733/480
Resumo: Abstract: Arjunolic acid (AA) obtained from plants of the Combretaceae family has shown anti-diabetic effects. Here, we analyzed whether the diabetogenic effects of dexamethasone (DEX) treatment on glucose homeostasis may be prevented or attenuated by the concomitant administration of AA. Adult Wistar rats were assigned to the following groups: vehicle-treated (Ctl), DEX-treated (1 mg/kg body weight intraperitoneally for 5 days) (Dex), AA-treated (30 mg/kg body weight by oral gavage twice per day) (Aa), AA treatment previous to and concomitant to DEX treatment (AaDex), and AA treatment after initiation of DEX treatment (DexAa). AA administration significantly ameliorated (AaDex) (P>0.05), but did not attenuate (DexAa), the glucose intolerance induced by DEX treatment. AA did not prevent or attenuate the elevation in hepatic glycogen and triacylglycerol content caused by DEX treatment. All DEX-treated rats exhibited hepatic steatosis that seemed to be more pronounced when associated with AA treatment given for a prolonged period (AaDex). Markers of liver function and oxidative stress were not significantly altered among the groups. Therefore, AA administered for a prolonged period partially prevents the glucose intolerance induced by DEX treatment, but it fails to produce this beneficial effect when given after initiation of GC treatment. Since AA may promote further hepatic steatosis when co-administered with GCs, care is required when considering this phytochemical as a hypoglycemiant and/or insulin-sensitizing agent
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spelling Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acidGlicocorticoidesGlucocorticoidsArjunolic acidGlucose toleranceInsulin sensitivityMetabolismArtigo originalAbstract: Arjunolic acid (AA) obtained from plants of the Combretaceae family has shown anti-diabetic effects. Here, we analyzed whether the diabetogenic effects of dexamethasone (DEX) treatment on glucose homeostasis may be prevented or attenuated by the concomitant administration of AA. Adult Wistar rats were assigned to the following groups: vehicle-treated (Ctl), DEX-treated (1 mg/kg body weight intraperitoneally for 5 days) (Dex), AA-treated (30 mg/kg body weight by oral gavage twice per day) (Aa), AA treatment previous to and concomitant to DEX treatment (AaDex), and AA treatment after initiation of DEX treatment (DexAa). AA administration significantly ameliorated (AaDex) (P>0.05), but did not attenuate (DexAa), the glucose intolerance induced by DEX treatment. AA did not prevent or attenuate the elevation in hepatic glycogen and triacylglycerol content caused by DEX treatment. All DEX-treated rats exhibited hepatic steatosis that seemed to be more pronounced when associated with AA treatment given for a prolonged period (AaDex). Markers of liver function and oxidative stress were not significantly altered among the groups. Therefore, AA administered for a prolonged period partially prevents the glucose intolerance induced by DEX treatment, but it fails to produce this beneficial effect when given after initiation of GC treatment. Since AA may promote further hepatic steatosis when co-administered with GCs, care is required when considering this phytochemical as a hypoglycemiant and/or insulin-sensitizing agentCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPAbertoUNIVERSIDADE ESTADUAL DE CAMPINASBoschero, Antonio Carlos, 1943-2014info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.12733/480BOSCHERO, Antonio Carlos. Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid. Indian journal of experimental biology. New Delhi : National Institute of Science Communication and Information Resources, 2014. Vol. 52, n. 10 (Oc., 2014), p. 972-982. Disponível em: https://hdl.handle.net/20.500.12733/480. Acesso em: 24 mai. 2023.Inglêshttps://repositorio.unicamp.br/acervo/detalhe/1231655reponame:Repositório da Produção Científica e Intelectual da Unicampinstname:Universidade Estadual de Campinas (UNICAMP)instacron:UNICAMPinfo:eu-repo/semantics/openAccess2021-11-12T12:14:57Zoai:https://www.repositorio.unicamp.br/:1231655Repositório InstitucionalPUBhttp://repositorio.unicamp.br/oai/requestreposip@unicamp.bropendoar:2021-11-12T12:14:57Repositório da Produção Científica e Intelectual da Unicamp - Universidade Estadual de Campinas (UNICAMP)false
dc.title.none.fl_str_mv Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
title Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
spellingShingle Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
Boschero, Antonio Carlos, 1943-
Glicocorticoides
Glucocorticoids
Arjunolic acid
Glucose tolerance
Insulin sensitivity
Metabolism
Artigo original
title_short Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
title_full Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
title_fullStr Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
title_full_unstemmed Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
title_sort Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
author Boschero, Antonio Carlos, 1943-
author_facet Boschero, Antonio Carlos, 1943-
author_role author
dc.contributor.none.fl_str_mv UNIVERSIDADE ESTADUAL DE CAMPINAS
dc.contributor.author.fl_str_mv Boschero, Antonio Carlos, 1943-
dc.subject.por.fl_str_mv Glicocorticoides
Glucocorticoids
Arjunolic acid
Glucose tolerance
Insulin sensitivity
Metabolism
Artigo original
topic Glicocorticoides
Glucocorticoids
Arjunolic acid
Glucose tolerance
Insulin sensitivity
Metabolism
Artigo original
description Abstract: Arjunolic acid (AA) obtained from plants of the Combretaceae family has shown anti-diabetic effects. Here, we analyzed whether the diabetogenic effects of dexamethasone (DEX) treatment on glucose homeostasis may be prevented or attenuated by the concomitant administration of AA. Adult Wistar rats were assigned to the following groups: vehicle-treated (Ctl), DEX-treated (1 mg/kg body weight intraperitoneally for 5 days) (Dex), AA-treated (30 mg/kg body weight by oral gavage twice per day) (Aa), AA treatment previous to and concomitant to DEX treatment (AaDex), and AA treatment after initiation of DEX treatment (DexAa). AA administration significantly ameliorated (AaDex) (P>0.05), but did not attenuate (DexAa), the glucose intolerance induced by DEX treatment. AA did not prevent or attenuate the elevation in hepatic glycogen and triacylglycerol content caused by DEX treatment. All DEX-treated rats exhibited hepatic steatosis that seemed to be more pronounced when associated with AA treatment given for a prolonged period (AaDex). Markers of liver function and oxidative stress were not significantly altered among the groups. Therefore, AA administered for a prolonged period partially prevents the glucose intolerance induced by DEX treatment, but it fails to produce this beneficial effect when given after initiation of GC treatment. Since AA may promote further hepatic steatosis when co-administered with GCs, care is required when considering this phytochemical as a hypoglycemiant and/or insulin-sensitizing agent
publishDate 2014
dc.date.none.fl_str_mv 2014
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 https://hdl.handle.net/20.500.12733/480
BOSCHERO, Antonio Carlos. Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid. Indian journal of experimental biology. New Delhi : National Institute of Science Communication and Information Resources, 2014. Vol. 52, n. 10 (Oc., 2014), p. 972-982. Disponível em: https://hdl.handle.net/20.500.12733/480. Acesso em: 24 mai. 2023.
url https://hdl.handle.net/20.500.12733/480
identifier_str_mv BOSCHERO, Antonio Carlos. Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid. Indian journal of experimental biology. New Delhi : National Institute of Science Communication and Information Resources, 2014. Vol. 52, n. 10 (Oc., 2014), p. 972-982. Disponível em: https://hdl.handle.net/20.500.12733/480. Acesso em: 24 mai. 2023.
dc.language.iso.fl_str_mv Inglês
language_invalid_str_mv Inglês
dc.relation.none.fl_str_mv https://repositorio.unicamp.br/acervo/detalhe/1231655
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.source.none.fl_str_mv reponame:Repositório da Produção Científica e Intelectual da Unicamp
instname:Universidade Estadual de Campinas (UNICAMP)
instacron:UNICAMP
instname_str Universidade Estadual de Campinas (UNICAMP)
instacron_str UNICAMP
institution UNICAMP
reponame_str Repositório da Produção Científica e Intelectual da Unicamp
collection Repositório da Produção Científica e Intelectual da Unicamp
repository.name.fl_str_mv Repositório da Produção Científica e Intelectual da Unicamp - Universidade Estadual de Campinas (UNICAMP)
repository.mail.fl_str_mv reposip@unicamp.br
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