Possible modulatory effect of endogenous islet catecholamines on insulin secretion

Autores
Borelli, María Inés; Gagliardino, Juan José
Año de publicación
2001
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: The possible participation of endogenous islet catecholamines (CAs) in the control of insulin secretion was tested. Methods: Glucose-induced insulin secretion was measured in the presence of 3-lodo-L-Tyrosine (MIT), a specific inhibitor of tyrosine-hydroxylase activity, in fresh and precultured islets isolated from normal rats. Incubated islets were also used to measure CAs release in the presence of low and high glucose, and the effect of α 2-(yohimbine [Y] and idazoxan [I]) and α1-adrenergic antagonists (prazosin [P] and terazosin [T]) upon insulin secretion elicited by high glucose. Results: Fresh islets incubated with 16.7 mM glucose released significantly more insulin in the presence of 1 μM MIT (6.66 ± 0.39 vs 5.01 ± 0.43 ng/islet/h, p < 0.02), but did not affect significantly the insulin response to low glucose. A similar enhancing effect of MIT upon insulin secretion was obtained using precultured islets devoid of neural cells, but absolute values were lower than those from fresh islets, suggesting that MIT inhibits islet rather than neural tyrosine hydroxylase. CAs concentration in the incubation media of fresh isolated islets was significantly higher in the presence of 16.7 than 3.3 mM glucose: dopamine 1.67 ± 0.13 vs 0.69 ± 0.13 pg/islet/h, p < 0.001, and noradrenaline 1.25 ± 0.17 vs 0.49 ± 0.04 pg/islet/h, p < 0.02. Y and I enhanced the release of insulin elicited by 16.7 mM glucose while P and T decreased such secretion. Conclusion: Our results suggest that islet-originated CAs directly modulate insulin release in a paracrine manner.
Facultad de Ciencias Médicas
Materia
Ciencias Médicas
catecholamine
idazoxan
iodotyrosine
noradrenalin
prazosin
terazosin
enzyme activity
pancreas islet cell
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/3.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/34608

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oai_identifier_str oai:sedici.unlp.edu.ar:10915/34608
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Possible modulatory effect of endogenous islet catecholamines on insulin secretionBorelli, María InésGagliardino, Juan JoséCiencias Médicascatecholamineidazoxaniodotyrosinenoradrenalinprazosinterazosinenzyme activitypancreas islet cellBackground: The possible participation of endogenous islet catecholamines (CAs) in the control of insulin secretion was tested. Methods: Glucose-induced insulin secretion was measured in the presence of 3-lodo-L-Tyrosine (MIT), a specific inhibitor of tyrosine-hydroxylase activity, in fresh and precultured islets isolated from normal rats. Incubated islets were also used to measure CAs release in the presence of low and high glucose, and the effect of α 2-(yohimbine [Y] and idazoxan [I]) and α1-adrenergic antagonists (prazosin [P] and terazosin [T]) upon insulin secretion elicited by high glucose. Results: Fresh islets incubated with 16.7 mM glucose released significantly more insulin in the presence of 1 μM MIT (6.66 ± 0.39 vs 5.01 ± 0.43 ng/islet/h, p < 0.02), but did not affect significantly the insulin response to low glucose. A similar enhancing effect of MIT upon insulin secretion was obtained using precultured islets devoid of neural cells, but absolute values were lower than those from fresh islets, suggesting that MIT inhibits islet rather than neural tyrosine hydroxylase. CAs concentration in the incubation media of fresh isolated islets was significantly higher in the presence of 16.7 than 3.3 mM glucose: dopamine 1.67 ± 0.13 vs 0.69 ± 0.13 pg/islet/h, p < 0.001, and noradrenaline 1.25 ± 0.17 vs 0.49 ± 0.04 pg/islet/h, p < 0.02. Y and I enhanced the release of insulin elicited by 16.7 mM glucose while P and T decreased such secretion. Conclusion: Our results suggest that islet-originated CAs directly modulate insulin release in a paracrine manner.Facultad de Ciencias Médicas2001-10-17info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/34608enginfo:eu-repo/semantics/altIdentifier/url/http://www.biomedcentral.com/content/pdf/1472-6823-1-1.pdfinfo:eu-repo/semantics/altIdentifier/issn/1472-6823info:eu-repo/semantics/altIdentifier/doi/10.1186/1472-6823-1-1info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/3.0/Creative Commons Attribution 3.0 Unported (CC BY 3.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-10-15T10:49:36Zoai:sedici.unlp.edu.ar:10915/34608Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-10-15 10:49:37.192SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Possible modulatory effect of endogenous islet catecholamines on insulin secretion
title Possible modulatory effect of endogenous islet catecholamines on insulin secretion
spellingShingle Possible modulatory effect of endogenous islet catecholamines on insulin secretion
Borelli, María Inés
Ciencias Médicas
catecholamine
idazoxan
iodotyrosine
noradrenalin
prazosin
terazosin
enzyme activity
pancreas islet cell
title_short Possible modulatory effect of endogenous islet catecholamines on insulin secretion
title_full Possible modulatory effect of endogenous islet catecholamines on insulin secretion
title_fullStr Possible modulatory effect of endogenous islet catecholamines on insulin secretion
title_full_unstemmed Possible modulatory effect of endogenous islet catecholamines on insulin secretion
title_sort Possible modulatory effect of endogenous islet catecholamines on insulin secretion
dc.creator.none.fl_str_mv Borelli, María Inés
Gagliardino, Juan José
author Borelli, María Inés
author_facet Borelli, María Inés
Gagliardino, Juan José
author_role author
author2 Gagliardino, Juan José
author2_role author
dc.subject.none.fl_str_mv Ciencias Médicas
catecholamine
idazoxan
iodotyrosine
noradrenalin
prazosin
terazosin
enzyme activity
pancreas islet cell
topic Ciencias Médicas
catecholamine
idazoxan
iodotyrosine
noradrenalin
prazosin
terazosin
enzyme activity
pancreas islet cell
dc.description.none.fl_txt_mv Background: The possible participation of endogenous islet catecholamines (CAs) in the control of insulin secretion was tested. Methods: Glucose-induced insulin secretion was measured in the presence of 3-lodo-L-Tyrosine (MIT), a specific inhibitor of tyrosine-hydroxylase activity, in fresh and precultured islets isolated from normal rats. Incubated islets were also used to measure CAs release in the presence of low and high glucose, and the effect of α 2-(yohimbine [Y] and idazoxan [I]) and α1-adrenergic antagonists (prazosin [P] and terazosin [T]) upon insulin secretion elicited by high glucose. Results: Fresh islets incubated with 16.7 mM glucose released significantly more insulin in the presence of 1 μM MIT (6.66 ± 0.39 vs 5.01 ± 0.43 ng/islet/h, p < 0.02), but did not affect significantly the insulin response to low glucose. A similar enhancing effect of MIT upon insulin secretion was obtained using precultured islets devoid of neural cells, but absolute values were lower than those from fresh islets, suggesting that MIT inhibits islet rather than neural tyrosine hydroxylase. CAs concentration in the incubation media of fresh isolated islets was significantly higher in the presence of 16.7 than 3.3 mM glucose: dopamine 1.67 ± 0.13 vs 0.69 ± 0.13 pg/islet/h, p < 0.001, and noradrenaline 1.25 ± 0.17 vs 0.49 ± 0.04 pg/islet/h, p < 0.02. Y and I enhanced the release of insulin elicited by 16.7 mM glucose while P and T decreased such secretion. Conclusion: Our results suggest that islet-originated CAs directly modulate insulin release in a paracrine manner.
Facultad de Ciencias Médicas
description Background: The possible participation of endogenous islet catecholamines (CAs) in the control of insulin secretion was tested. Methods: Glucose-induced insulin secretion was measured in the presence of 3-lodo-L-Tyrosine (MIT), a specific inhibitor of tyrosine-hydroxylase activity, in fresh and precultured islets isolated from normal rats. Incubated islets were also used to measure CAs release in the presence of low and high glucose, and the effect of α 2-(yohimbine [Y] and idazoxan [I]) and α1-adrenergic antagonists (prazosin [P] and terazosin [T]) upon insulin secretion elicited by high glucose. Results: Fresh islets incubated with 16.7 mM glucose released significantly more insulin in the presence of 1 μM MIT (6.66 ± 0.39 vs 5.01 ± 0.43 ng/islet/h, p < 0.02), but did not affect significantly the insulin response to low glucose. A similar enhancing effect of MIT upon insulin secretion was obtained using precultured islets devoid of neural cells, but absolute values were lower than those from fresh islets, suggesting that MIT inhibits islet rather than neural tyrosine hydroxylase. CAs concentration in the incubation media of fresh isolated islets was significantly higher in the presence of 16.7 than 3.3 mM glucose: dopamine 1.67 ± 0.13 vs 0.69 ± 0.13 pg/islet/h, p < 0.001, and noradrenaline 1.25 ± 0.17 vs 0.49 ± 0.04 pg/islet/h, p < 0.02. Y and I enhanced the release of insulin elicited by 16.7 mM glucose while P and T decreased such secretion. Conclusion: Our results suggest that islet-originated CAs directly modulate insulin release in a paracrine manner.
publishDate 2001
dc.date.none.fl_str_mv 2001-10-17
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/34608
url http://sedici.unlp.edu.ar/handle/10915/34608
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.biomedcentral.com/content/pdf/1472-6823-1-1.pdf
info:eu-repo/semantics/altIdentifier/issn/1472-6823
info:eu-repo/semantics/altIdentifier/doi/10.1186/1472-6823-1-1
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/3.0/
Creative Commons Attribution 3.0 Unported (CC BY 3.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/3.0/
Creative Commons Attribution 3.0 Unported (CC BY 3.0)
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
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reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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