Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine

Detalhes bibliográficos
Autor(a) principal: Mendonça, A.C.
Data de Publicação: 1998
Outros Autores: Carneiro, E.M. [UNESP], Bosqueiro, J.R. [UNESP], Crepaldi-Alves, S.C. [UNESP], Boschero, A.C.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
DOI: 10.1590/S0100-879X1998000600018
Texto Completo: http://dx.doi.org/10.1590/S0100-879X1998000600018
http://hdl.handle.net/11449/20638
Resumo: We studied the development of the insulin secretion mechanism in the pancreas of fetal (19- and 21-day-old), neonatal (3-day-old), and adult (90-day-old) rats in response to stimulation with 8.3 or 16.7 mM glucose, 30 mM K+, 5 mM theophylline (Theo) and 200 µM carbamylcholine (Cch). No effect of glucose or high K+ was observed on the pancreas from 19-day-old fetuses, whereas Theo and Cch significantly increased insulin secretion at this age (82 and 127% above basal levels, respectively). High K+ also failed to alter the insulin secretion in the pancreas from 21-day-old fetuses, whereas 8.3 mM and 16.7 mM glucose significantly stimulated insulin release by 41 and 54% above basal levels, respectively. Similar results were obtained with Theo and Cch. A more marked effect of glucose on insulin secretion was observed in the pancreas of 3-day-old rats, reaching 84 and 179% above basal levels with 8.3 mM and 16.7 mM glucose, respectively. At this age, both Theo and Cch increased insulin secretion to close to two-times basal levels. In islets from adult rats, 8.3 mM and 16.7 mM glucose, Theo, and Cch increased the insulin release by 104, 193, 318 and 396% above basal levels, respectively. These data indicate that pancreatic B-cells from 19-day-old fetuses were already sensitive to stimuli that use either cAMP or IP3 and DAG as second messengers, but insensitive to stimuli such as glucose and high K+ that induce membrane depolarization. The greater effect of glucose on insulin secretion during the neonatal period indicates that this period is crucial for the maturation of the glucose-sensing mechanism in B-cells.
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spelling Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholinerat islet cellglucosepancreatic isletscarbamylcholinetheophyllinepotassiuminsulin secretionWe studied the development of the insulin secretion mechanism in the pancreas of fetal (19- and 21-day-old), neonatal (3-day-old), and adult (90-day-old) rats in response to stimulation with 8.3 or 16.7 mM glucose, 30 mM K+, 5 mM theophylline (Theo) and 200 µM carbamylcholine (Cch). No effect of glucose or high K+ was observed on the pancreas from 19-day-old fetuses, whereas Theo and Cch significantly increased insulin secretion at this age (82 and 127% above basal levels, respectively). High K+ also failed to alter the insulin secretion in the pancreas from 21-day-old fetuses, whereas 8.3 mM and 16.7 mM glucose significantly stimulated insulin release by 41 and 54% above basal levels, respectively. Similar results were obtained with Theo and Cch. A more marked effect of glucose on insulin secretion was observed in the pancreas of 3-day-old rats, reaching 84 and 179% above basal levels with 8.3 mM and 16.7 mM glucose, respectively. At this age, both Theo and Cch increased insulin secretion to close to two-times basal levels. In islets from adult rats, 8.3 mM and 16.7 mM glucose, Theo, and Cch increased the insulin release by 104, 193, 318 and 396% above basal levels, respectively. These data indicate that pancreatic B-cells from 19-day-old fetuses were already sensitive to stimuli that use either cAMP or IP3 and DAG as second messengers, but insensitive to stimuli such as glucose and high K+ that induce membrane depolarization. The greater effect of glucose on insulin secretion during the neonatal period indicates that this period is crucial for the maturation of the glucose-sensing mechanism in B-cells.Universidade Estadual de CampinasUniversidade Estadual PaulistaUniversidade Estadual PaulistaAssociação Brasileira de Divulgação Científica (ABRADIC)Universidade Estadual de Campinas (UNICAMP)Universidade Estadual Paulista (Unesp)Mendonça, A.C.Carneiro, E.M. [UNESP]Bosqueiro, J.R. [UNESP]Crepaldi-Alves, S.C. [UNESP]Boschero, A.C.2013-09-30T19:43:58Z2014-05-20T13:57:56Z2013-09-30T19:43:58Z2014-05-20T13:57:56Z1998-06-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article841-846application/pdfhttp://dx.doi.org/10.1590/S0100-879X1998000600018Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 31, n. 6, p. 841-846, 1998.0100-879Xhttp://hdl.handle.net/11449/2063810.1590/S0100-879X1998000600018S0100-879X1998000600018S0100-879X1998000600018.pdfSciELOreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengBrazilian Journal of Medical and Biological Research1.492info:eu-repo/semantics/openAccess2023-10-25T06:07:34Zoai:repositorio.unesp.br:11449/20638Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T15:53:27.752794Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
title Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
spellingShingle Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
Mendonça, A.C.
rat islet cell
glucose
pancreatic islets
carbamylcholine
theophylline
potassium
insulin secretion
Mendonça, A.C.
rat islet cell
glucose
pancreatic islets
carbamylcholine
theophylline
potassium
insulin secretion
title_short Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
title_full Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
title_fullStr Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
title_full_unstemmed Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
title_sort Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
author Mendonça, A.C.
author_facet Mendonça, A.C.
Mendonça, A.C.
Carneiro, E.M. [UNESP]
Bosqueiro, J.R. [UNESP]
Crepaldi-Alves, S.C. [UNESP]
Boschero, A.C.
Carneiro, E.M. [UNESP]
Bosqueiro, J.R. [UNESP]
Crepaldi-Alves, S.C. [UNESP]
Boschero, A.C.
author_role author
author2 Carneiro, E.M. [UNESP]
Bosqueiro, J.R. [UNESP]
Crepaldi-Alves, S.C. [UNESP]
Boschero, A.C.
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual de Campinas (UNICAMP)
Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Mendonça, A.C.
Carneiro, E.M. [UNESP]
Bosqueiro, J.R. [UNESP]
Crepaldi-Alves, S.C. [UNESP]
Boschero, A.C.
dc.subject.por.fl_str_mv rat islet cell
glucose
pancreatic islets
carbamylcholine
theophylline
potassium
insulin secretion
topic rat islet cell
glucose
pancreatic islets
carbamylcholine
theophylline
potassium
insulin secretion
description We studied the development of the insulin secretion mechanism in the pancreas of fetal (19- and 21-day-old), neonatal (3-day-old), and adult (90-day-old) rats in response to stimulation with 8.3 or 16.7 mM glucose, 30 mM K+, 5 mM theophylline (Theo) and 200 µM carbamylcholine (Cch). No effect of glucose or high K+ was observed on the pancreas from 19-day-old fetuses, whereas Theo and Cch significantly increased insulin secretion at this age (82 and 127% above basal levels, respectively). High K+ also failed to alter the insulin secretion in the pancreas from 21-day-old fetuses, whereas 8.3 mM and 16.7 mM glucose significantly stimulated insulin release by 41 and 54% above basal levels, respectively. Similar results were obtained with Theo and Cch. A more marked effect of glucose on insulin secretion was observed in the pancreas of 3-day-old rats, reaching 84 and 179% above basal levels with 8.3 mM and 16.7 mM glucose, respectively. At this age, both Theo and Cch increased insulin secretion to close to two-times basal levels. In islets from adult rats, 8.3 mM and 16.7 mM glucose, Theo, and Cch increased the insulin release by 104, 193, 318 and 396% above basal levels, respectively. These data indicate that pancreatic B-cells from 19-day-old fetuses were already sensitive to stimuli that use either cAMP or IP3 and DAG as second messengers, but insensitive to stimuli such as glucose and high K+ that induce membrane depolarization. The greater effect of glucose on insulin secretion during the neonatal period indicates that this period is crucial for the maturation of the glucose-sensing mechanism in B-cells.
publishDate 1998
dc.date.none.fl_str_mv 1998-06-01
2013-09-30T19:43:58Z
2013-09-30T19:43:58Z
2014-05-20T13:57:56Z
2014-05-20T13:57:56Z
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 http://dx.doi.org/10.1590/S0100-879X1998000600018
Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 31, n. 6, p. 841-846, 1998.
0100-879X
http://hdl.handle.net/11449/20638
10.1590/S0100-879X1998000600018
S0100-879X1998000600018
S0100-879X1998000600018.pdf
url http://dx.doi.org/10.1590/S0100-879X1998000600018
http://hdl.handle.net/11449/20638
identifier_str_mv Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 31, n. 6, p. 841-846, 1998.
0100-879X
10.1590/S0100-879X1998000600018
S0100-879X1998000600018
S0100-879X1998000600018.pdf
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Brazilian Journal of Medical and Biological Research
1.492
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 841-846
application/pdf
dc.publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica (ABRADIC)
publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica (ABRADIC)
dc.source.none.fl_str_mv SciELO
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
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dc.identifier.doi.none.fl_str_mv 10.1590/S0100-879X1998000600018