Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.

The local synthesis of dopamine and its effects on insulin release have been described in isolated islets. Thus, it may be accepted that dopamine exerts an auto-paracrine regulation of insulin secretion from pancreatic beta cells. The aim of the present study is to analyze whether dopamine is a regu...

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Main Authors: Maria Jose Garcia Barrado, Maria Carmen Iglesias Osma, Enrique J Blanco, Marta Carretero Hernández, Virginia Sánchez Robledo, Leonardo Catalano Iniesta, Sixto Carrero, Jose Carretero
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4401745?pdf=render
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spelling doaj-253e0fc8f70a4ce9b4c3862881d569492020-11-25T02:47:07ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01104e012319710.1371/journal.pone.0123197Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.Maria Jose Garcia BarradoMaria Carmen Iglesias OsmaEnrique J BlancoMarta Carretero HernándezVirginia Sánchez RobledoLeonardo Catalano IniestaSixto CarreroJose CarreteroThe local synthesis of dopamine and its effects on insulin release have been described in isolated islets. Thus, it may be accepted that dopamine exerts an auto-paracrine regulation of insulin secretion from pancreatic beta cells. The aim of the present study is to analyze whether dopamine is a regulator of the proliferation and apoptosis of rat pancreatic beta cells after glucose-stimulated insulin secretion. Glucose stimulated pancreatic islets obtained from male Wistar rats were cultured with 1 or 10 μM dopamine from 1 to 12 h. Insulin secretion was analyzed by RIA. The cellular proliferation rate of pancreatic islets and beta cells was studied with immunocytochemical double labelling for both insulin and PCNA (proliferating cell nuclear antigen), and active caspase-3 was detected to evaluate apoptosis. The secretion of insulin from isolated islets was significantly inhibited (p<0.01), by treatment with 1 and 10 μM dopamine, with no differences between either dose as early as 1 h after treatment. The percentage of insulin-positive cells in the islets decreased significantly (p<0.01) after 1 h of treatment up to 12 h. The proliferation rate of insulin-positive cells in the islets decreased significantly (p<0.01) following treatment with dopamine. Apoptosis in pancreatic islets and beta cells was increased by treatment with 1 and 10 μM dopamine along 12 h. In conclusion, these results suggest that dopamine could modulate the proliferation and apoptosis of pancreatic beta cells and that dopamine may be involved in the maintenance of pancreatic islets.http://europepmc.org/articles/PMC4401745?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Maria Jose Garcia Barrado
Maria Carmen Iglesias Osma
Enrique J Blanco
Marta Carretero Hernández
Virginia Sánchez Robledo
Leonardo Catalano Iniesta
Sixto Carrero
Jose Carretero
spellingShingle Maria Jose Garcia Barrado
Maria Carmen Iglesias Osma
Enrique J Blanco
Marta Carretero Hernández
Virginia Sánchez Robledo
Leonardo Catalano Iniesta
Sixto Carrero
Jose Carretero
Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.
PLoS ONE
author_facet Maria Jose Garcia Barrado
Maria Carmen Iglesias Osma
Enrique J Blanco
Marta Carretero Hernández
Virginia Sánchez Robledo
Leonardo Catalano Iniesta
Sixto Carrero
Jose Carretero
author_sort Maria Jose Garcia Barrado
title Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.
title_short Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.
title_full Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.
title_fullStr Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.
title_full_unstemmed Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.
title_sort dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2015-01-01
description The local synthesis of dopamine and its effects on insulin release have been described in isolated islets. Thus, it may be accepted that dopamine exerts an auto-paracrine regulation of insulin secretion from pancreatic beta cells. The aim of the present study is to analyze whether dopamine is a regulator of the proliferation and apoptosis of rat pancreatic beta cells after glucose-stimulated insulin secretion. Glucose stimulated pancreatic islets obtained from male Wistar rats were cultured with 1 or 10 μM dopamine from 1 to 12 h. Insulin secretion was analyzed by RIA. The cellular proliferation rate of pancreatic islets and beta cells was studied with immunocytochemical double labelling for both insulin and PCNA (proliferating cell nuclear antigen), and active caspase-3 was detected to evaluate apoptosis. The secretion of insulin from isolated islets was significantly inhibited (p<0.01), by treatment with 1 and 10 μM dopamine, with no differences between either dose as early as 1 h after treatment. The percentage of insulin-positive cells in the islets decreased significantly (p<0.01) after 1 h of treatment up to 12 h. The proliferation rate of insulin-positive cells in the islets decreased significantly (p<0.01) following treatment with dopamine. Apoptosis in pancreatic islets and beta cells was increased by treatment with 1 and 10 μM dopamine along 12 h. In conclusion, these results suggest that dopamine could modulate the proliferation and apoptosis of pancreatic beta cells and that dopamine may be involved in the maintenance of pancreatic islets.
url http://europepmc.org/articles/PMC4401745?pdf=render
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