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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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Effects of dopamine on insulin content and release.(A) Inhibition of insulin secretion in overnight cultured rat islets followed by treatment in glucose with dopamine 1 μM and 10 μM contrasted with glucose 10 mM as a control. Insulin secretion was then monitored at 1, 3, 6 and 12 h. (B) Absolute values AUC of insulin secretion were calculated for 10 mM glucose, 1μM and 10μM dopamine. (C) The insulin content of the islets used to study insulin secretion was determined at the end of the culture at 1, 3, 6 and 12h. (D) Absolute values of AUC of insulin content were calculated for 10 mM glucose and 1μM and 10μM dopamine. (E) This shows the sum AUC of insulin content (inferior portion) and insulin secretion (superior portion) by the same islets during treatment with dopamine (1 and 10 μM) versus glucose 10 mM. Absolute values are represented as means ± SEM for 15 batches of islets (10 islets per batch) from 2 experiments (*p<0.05 and **p<0.01).
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pone.0123197.g001: Effects of dopamine on insulin content and release.(A) Inhibition of insulin secretion in overnight cultured rat islets followed by treatment in glucose with dopamine 1 μM and 10 μM contrasted with glucose 10 mM as a control. Insulin secretion was then monitored at 1, 3, 6 and 12 h. (B) Absolute values AUC of insulin secretion were calculated for 10 mM glucose, 1μM and 10μM dopamine. (C) The insulin content of the islets used to study insulin secretion was determined at the end of the culture at 1, 3, 6 and 12h. (D) Absolute values of AUC of insulin content were calculated for 10 mM glucose and 1μM and 10μM dopamine. (E) This shows the sum AUC of insulin content (inferior portion) and insulin secretion (superior portion) by the same islets during treatment with dopamine (1 and 10 μM) versus glucose 10 mM. Absolute values are represented as means ± SEM for 15 batches of islets (10 islets per batch) from 2 experiments (*p<0.05 and **p<0.01).

Mentions: Fig 1A shows the insulin levels in the culture medium from 1 h to 12 h following incubation with 10mM glucose. The insulin-levels in the medium ranged from 11.4±0.8 to 83.9±5.8 ng/islet, with a significant increase (p<0.01) at 3, 6 and 12 h in comparison with 1 h. The area under the curve (AUC) (Fig 1B) under the same conditions was 749.4± 48.3 ng/islet/12h. Treatment with dopamine induced a reduction in insulin release to the medium at all times and for all doses assayed (at 1, 3 and 6 h p<0.01 and at 12 h p<0.05 versus 10 mM glucose). The AUC of insulin secretion with time was decreased by about 25% for both doses of dopamine (p<0.01 n = 4, Fig 1B).


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)

Effects of dopamine on insulin content and release.(A) Inhibition of insulin secretion in overnight cultured rat islets followed by treatment in glucose with dopamine 1 μM and 10 μM contrasted with glucose 10 mM as a control. Insulin secretion was then monitored at 1, 3, 6 and 12 h. (B) Absolute values AUC of insulin secretion were calculated for 10 mM glucose, 1μM and 10μM dopamine. (C) The insulin content of the islets used to study insulin secretion was determined at the end of the culture at 1, 3, 6 and 12h. (D) Absolute values of AUC of insulin content were calculated for 10 mM glucose and 1μM and 10μM dopamine. (E) This shows the sum AUC of insulin content (inferior portion) and insulin secretion (superior portion) by the same islets during treatment with dopamine (1 and 10 μM) versus glucose 10 mM. Absolute values are represented as means ± SEM for 15 batches of islets (10 islets per batch) from 2 experiments (*p<0.05 and **p<0.01).
© Copyright Policy
Related In: Results  -  Collection

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

pone.0123197.g001: Effects of dopamine on insulin content and release.(A) Inhibition of insulin secretion in overnight cultured rat islets followed by treatment in glucose with dopamine 1 μM and 10 μM contrasted with glucose 10 mM as a control. Insulin secretion was then monitored at 1, 3, 6 and 12 h. (B) Absolute values AUC of insulin secretion were calculated for 10 mM glucose, 1μM and 10μM dopamine. (C) The insulin content of the islets used to study insulin secretion was determined at the end of the culture at 1, 3, 6 and 12h. (D) Absolute values of AUC of insulin content were calculated for 10 mM glucose and 1μM and 10μM dopamine. (E) This shows the sum AUC of insulin content (inferior portion) and insulin secretion (superior portion) by the same islets during treatment with dopamine (1 and 10 μM) versus glucose 10 mM. Absolute values are represented as means ± SEM for 15 batches of islets (10 islets per batch) from 2 experiments (*p<0.05 and **p<0.01).
Mentions: Fig 1A shows the insulin levels in the culture medium from 1 h to 12 h following incubation with 10mM glucose. The insulin-levels in the medium ranged from 11.4±0.8 to 83.9±5.8 ng/islet, with a significant increase (p<0.01) at 3, 6 and 12 h in comparison with 1 h. The area under the curve (AUC) (Fig 1B) under the same conditions was 749.4± 48.3 ng/islet/12h. Treatment with dopamine induced a reduction in insulin release to the medium at all times and for all doses assayed (at 1, 3 and 6 h p<0.01 and at 12 h p<0.05 versus 10 mM glucose). The AUC of insulin secretion with time was decreased by about 25% for both doses of dopamine (p<0.01 n = 4, Fig 1B).

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