Possible modulatory effect of endogenous islet catecholamines on insulin secretion

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 prec...

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Detalles Bibliográficos
Autores principales: Borelli, María Inés, Gagliardino, Juan José
Formato: Articulo
Lenguaje:Inglés
Publicado: 2001
Materias:
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/34608
http://www.biomedcentral.com/content/pdf/1472-6823-1-1.pdf
Aporte de:
id I19-R120-10915-34608
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Médicas
catecholamine
idazoxan
iodotyrosine
noradrenalin
prazosin
terazosin
enzyme activity
pancreas islet cell
spellingShingle Ciencias Médicas
catecholamine
idazoxan
iodotyrosine
noradrenalin
prazosin
terazosin
enzyme activity
pancreas islet cell
Borelli, María Inés
Gagliardino, Juan José
Possible modulatory effect of endogenous islet catecholamines on insulin secretion
topic_facet Ciencias Médicas
catecholamine
idazoxan
iodotyrosine
noradrenalin
prazosin
terazosin
enzyme activity
pancreas islet cell
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.
format Articulo
Articulo
author Borelli, María Inés
Gagliardino, Juan José
author_facet Borelli, María Inés
Gagliardino, Juan José
author_sort Borelli, María Inés
title Possible modulatory effect of endogenous islet catecholamines on insulin secretion
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
publishDate 2001
url http://sedici.unlp.edu.ar/handle/10915/34608
http://www.biomedcentral.com/content/pdf/1472-6823-1-1.pdf
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