ArticleBMC endocrine disorders2001
Possible modulatory effect of endogenous islet catecholamines on insulin secretion.
Article in BMC endocrine disorders, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.PloS one · 2015Article
- Vascular endothelial growth factor coordinates islet innervation via vascular scaffolding.Development (Cambridge, England) · 2014Article
- Role of vesicular monoamine transporter type 2 in rodent insulin secretion and glucose metabolism revealed by its specific antagonist tetrabenazine.The Journal of endocrinology · 2008Article
- VMAT2 gene expression and function as it applies to imaging beta-cell mass.Journal of molecular medicine (Berlin, Germany) · 2008Review
- Bromocriptine-induced hyperglycemia in nonobese diabetic mice: kinetics and mechanisms of action.The review of diabetic studies : RDS · 2007Article
- Comparison of c-Fos immunoreactivity in pancreatic beta cells and cells with neural crest, endoderm and mesoderm origin in rats.Journal of endocrinological investigation · 2004Article
- Tyrosine hydroxylase activity in the endocrine pancreas: changes induced by short-term dietary manipulation.BMC endocrine disorders · 2003Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe possible participation of endogenous islet catecholamines (CAs) in the control of insulin secretion was tested.
methodsGlucose-induced insulin secretion was measured in the presence of 3-Iodo-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 alpha2-(yohimbine [Y] and idazoxan [I]) and alpha1-adrenergic antagonists (prazosin [P] and terazosin [T]) upon insulin secretion elicited by high glucose.
resultsFresh islets incubated with 16.7 mM glucose released significantly more insulin in the presence of 1 &mgr;M 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.
conclusionOur results suggest that islet-originated CAs directly modulate insulin release in a paracrine manner.
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