Endothelin-1 stimulates insulin secretion by direct-action on the islets of Langerhans in mice
Diabetologia, ISSN: 0012-186X, Vol: 39, Issue: 9, Page: 1030-1035
1996
- 44Citations
- 16Captures
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Metrics Details
- Citations44
- Citation Indexes44
- 44
- CrossRef35
- Captures16
- Readers16
- 16
Article Description
Endothelin-1 (ET-1), a potent endothelium-derived vasoconstrictor peptide, is secreted in response to insulin. Elevated circulating ET-1 levels have been found in patients with diabetes mellitus and vascular dysfunction. The question arises whether ET-1 acts as a direct modulator of insulin secre tion. To test this, we studied the effects of ET-1 on isolated mouse islets of Langerhans. ET-1 (1 nmol/l-1 μmol/l) dose-dependently stimulated insulin secretion from islets incubated in the presence of 16.7 mmol/l glucose (p < 0.05). The effect of ET-1 is glucose-dependent since no potentiation was found at 3.3 mmol/l glucose. Furthermore, ET-1 induced a large, transient increase in glucose-stimulated insulin secretion during islet perifusion in the presence (p < 0.001), but not in the absence, of extracellular Ca. The rate of Ca-efflux from Ca-prelabelled islets was transiently stimulated by ET-1 during perifusion at 16.7 mmol/l glucose in the presence of extracellular Ca (p < 0.01). A short-lived increase in Ca -efflux was also observed in the absence of extracellular Ca (p < 0.05). It is suggested that the effects of ET-1 on insulin secretion are critically dependent on influx via Ca -channels. In addition, ET-1 transiently enhanced Rb+ -efflux from Rb -prelabelled islets both in the presence (p < 0.001) and in the absence (p < 0.001) of extracellular Ca' suggesting that ET-1 does not elicit insulin secretion by inhibition of the potassium permeability. Our study provides evidence that ET-1 stimulates insulin secretion via a direct effect on the islets of Langerhans.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0029813312&origin=inward; http://dx.doi.org/10.1007/bf00400650; http://www.ncbi.nlm.nih.gov/pubmed/8877285; http://www.springerlink.com/Index/10.1007/s001250050549; http://dx.doi.org/10.1007/s001250050549; http://link.springer.com/10.1007/BF00400650; http://www.springerlink.com/index/pdf/10.1007/BF00400650; https://dx.doi.org/10.1007/s001250050549; https://link.springer.com/article/10.1007/BF00400650; http://www.springerlink.com/index/10.1007/BF00400650; https://dx.doi.org/10.1007/bf00400650
Springer Nature
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