Disruption of glucose tolerance caused by glucocorticoid excess in rats is partially prevented, but not attenuated, by arjunolic acid
Autor(a) principal: | |
---|---|
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 |
id |
CAMP_10c172ba71465dc32827b360e175e289 |
---|---|
oai_identifier_str |
oai:https://www.repositorio.unicamp.br/:1231655 |
network_acronym_str |
CAMP |
network_name_str |
Repositório da Produção Científica e Intelectual da Unicamp |
repository_id_str |
|
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 |
_version_ |
1766887321881280512 |