Endothelin-1 stimulates insulin secretion by direct action on the islets of Langerhans in mice.

Søren Gregersen, Janus Laust Thomsen, Kjeld Hermansen

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Udgivelsesdato: Sep
OriginalsprogEngelsk
TidsskriftDiabetologia
Vol/bind39
Udgave nummer9
Sider (fra-til)1030-5
ISSN0012-186X
StatusUdgivet - 1. sep. 1996
Udgivet eksterntJa

Fingeraftryk

Endothelin-1
Islets of Langerhans
Insulin
Endothelium
Diabetes Mellitus
Potassium

Citer dette

Gregersen, S., Thomsen, J. L., & Hermansen, K. (1996). Endothelin-1 stimulates insulin secretion by direct action on the islets of Langerhans in mice. Diabetologia, 39(9), 1030-5.
Gregersen, Søren ; Thomsen, Janus Laust ; Hermansen, Kjeld. / Endothelin-1 stimulates insulin secretion by direct action on the islets of Langerhans in mice. I: Diabetologia. 1996 ; Bind 39, Nr. 9. s. 1030-5.
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title = "Endothelin-1 stimulates insulin secretion by direct action on the islets of Langerhans in mice.",
abstract = "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 secretion. To test this, we studied the effects of ET-1 on isolated mouse islets of Langerhans. ET-1 (1 nmol/l-1 mumol/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 Ca2+. The rate of 45Ca(2+)-efflux from 45Ca(2+)-prelabelled islets was transiently stimulated by ET-1 during perifusion at 16.7 mmol/l glucose in the presence of extracellular Ca2+ (p < 0.001). A short-lived increase in 45Ca(2+)-efflux was also observed in the absence of extracellular Ca2+ (p < 0.05). It is suggested that the effects of ET-1 on insulin secretion are critically dependent on influx via Ca(2+)-channels. In addition, ET-1 transiently enhanced 86Rb(+)-efflux from 86Rb(+)-prelabelled islets both in the presence (p < 0.001) and in the absence (p < 0.001) of extracellular Ca2+ 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.",
author = "S{\o}ren Gregersen and Thomsen, {Janus Laust} and Kjeld Hermansen",
year = "1996",
month = "9",
day = "1",
language = "English",
volume = "39",
pages = "1030--5",
journal = "Diabetologia",
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Gregersen, S, Thomsen, JL & Hermansen, K 1996, 'Endothelin-1 stimulates insulin secretion by direct action on the islets of Langerhans in mice.', Diabetologia, bind 39, nr. 9, s. 1030-5.

Endothelin-1 stimulates insulin secretion by direct action on the islets of Langerhans in mice. / Gregersen, Søren; Thomsen, Janus Laust; Hermansen, Kjeld.

I: Diabetologia, Bind 39, Nr. 9, 01.09.1996, s. 1030-5.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Endothelin-1 stimulates insulin secretion by direct action on the islets of Langerhans in mice.

AU - Gregersen, Søren

AU - Thomsen, Janus Laust

AU - Hermansen, Kjeld

PY - 1996/9/1

Y1 - 1996/9/1

N2 - 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 secretion. To test this, we studied the effects of ET-1 on isolated mouse islets of Langerhans. ET-1 (1 nmol/l-1 mumol/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 Ca2+. The rate of 45Ca(2+)-efflux from 45Ca(2+)-prelabelled islets was transiently stimulated by ET-1 during perifusion at 16.7 mmol/l glucose in the presence of extracellular Ca2+ (p < 0.001). A short-lived increase in 45Ca(2+)-efflux was also observed in the absence of extracellular Ca2+ (p < 0.05). It is suggested that the effects of ET-1 on insulin secretion are critically dependent on influx via Ca(2+)-channels. In addition, ET-1 transiently enhanced 86Rb(+)-efflux from 86Rb(+)-prelabelled islets both in the presence (p < 0.001) and in the absence (p < 0.001) of extracellular Ca2+ 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.

AB - 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 secretion. To test this, we studied the effects of ET-1 on isolated mouse islets of Langerhans. ET-1 (1 nmol/l-1 mumol/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 Ca2+. The rate of 45Ca(2+)-efflux from 45Ca(2+)-prelabelled islets was transiently stimulated by ET-1 during perifusion at 16.7 mmol/l glucose in the presence of extracellular Ca2+ (p < 0.001). A short-lived increase in 45Ca(2+)-efflux was also observed in the absence of extracellular Ca2+ (p < 0.05). It is suggested that the effects of ET-1 on insulin secretion are critically dependent on influx via Ca(2+)-channels. In addition, ET-1 transiently enhanced 86Rb(+)-efflux from 86Rb(+)-prelabelled islets both in the presence (p < 0.001) and in the absence (p < 0.001) of extracellular Ca2+ 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.

M3 - Journal article

VL - 39

SP - 1030

EP - 1035

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 9

ER -