Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine
Autor(a) principal: | |
---|---|
Data de Publicação: | 1998 |
Outros Autores: | , , , |
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. |
id |
UNSP_ae1e8aff764e7747ef4557fc18a2d215 |
---|---|
oai_identifier_str |
oai:repositorio.unesp.br:11449/20638 |
network_acronym_str |
UNSP |
network_name_str |
Repositório Institucional da UNESP |
repository_id_str |
2946 |
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 |
|
_version_ |
1822218543450554368 |
dc.identifier.doi.none.fl_str_mv |
10.1590/S0100-879X1998000600018 |