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

Garcia Barrado MJ, Iglesias Osma MC, Blanco EJ, Carretero Hernández M, Sánchez Robledo V, Catalano Iniesta L, Carrero S, Carretero J - PLoS ONE (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Faculty of Medicine, University of Salamanca, Salamanca, Spain; Laboratory of Neuroendocrinology, Institute of Neurosciences of Castilla y León, and Laboratory of Neuroendocrinology and Obesity of IBSAL, University of Salamanca, Salamanca, Spain.

ABSTRACT
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.

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Morphometric effect induced by treatment with dopamine on cellular (A) and nuclear (B) area of beta cells.Histological sections were selected from micrographs of cross sections of each islets (see methods). In each section the cellular and the nuclear cell profiles from insulin-positive cells were plotted, allowing the surface of the cell and nuclear areas to be calculated after calibration of the Image J application. Cellular and nuclear area from10 islets per study group, and 100cells per islet were measured in 10 mM glucose, 1μM and 10 μM dopamine. (area: μm2, **p<0.01).
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pone.0123197.g003: Morphometric effect induced by treatment with dopamine on cellular (A) and nuclear (B) area of beta cells.Histological sections were selected from micrographs of cross sections of each islets (see methods). In each section the cellular and the nuclear cell profiles from insulin-positive cells were plotted, allowing the surface of the cell and nuclear areas to be calculated after calibration of the Image J application. Cellular and nuclear area from10 islets per study group, and 100cells per islet were measured in 10 mM glucose, 1μM and 10 μM dopamine. (area: μm2, **p<0.01).

Mentions: In the islets, the presence of dopamine decreased the cellular (Fig 3A) and nuclear areas of insulin-positive cells significantly for all doses and time-points assayed (Fig 3B), with a reduction of approximately 30% in the cellular area (**p<0.01) and of 45% in the nuclear area.


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

Garcia Barrado MJ, Iglesias Osma MC, Blanco EJ, Carretero Hernández M, Sánchez Robledo V, Catalano Iniesta L, Carrero S, Carretero J - PLoS ONE (2015)

Morphometric effect induced by treatment with dopamine on cellular (A) and nuclear (B) area of beta cells.Histological sections were selected from micrographs of cross sections of each islets (see methods). In each section the cellular and the nuclear cell profiles from insulin-positive cells were plotted, allowing the surface of the cell and nuclear areas to be calculated after calibration of the Image J application. Cellular and nuclear area from10 islets per study group, and 100cells per islet were measured in 10 mM glucose, 1μM and 10 μM dopamine. (area: μm2, **p<0.01).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4401745&req=5

pone.0123197.g003: Morphometric effect induced by treatment with dopamine on cellular (A) and nuclear (B) area of beta cells.Histological sections were selected from micrographs of cross sections of each islets (see methods). In each section the cellular and the nuclear cell profiles from insulin-positive cells were plotted, allowing the surface of the cell and nuclear areas to be calculated after calibration of the Image J application. Cellular and nuclear area from10 islets per study group, and 100cells per islet were measured in 10 mM glucose, 1μM and 10 μM dopamine. (area: μm2, **p<0.01).
Mentions: In the islets, the presence of dopamine decreased the cellular (Fig 3A) and nuclear areas of insulin-positive cells significantly for all doses and time-points assayed (Fig 3B), with a reduction of approximately 30% in the cellular area (**p<0.01) and of 45% in the nuclear area.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Faculty of Medicine, University of Salamanca, Salamanca, Spain; Laboratory of Neuroendocrinology, Institute of Neurosciences of Castilla y León, and Laboratory of Neuroendocrinology and Obesity of IBSAL, University of Salamanca, Salamanca, Spain.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus