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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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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