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Pulses of somatostatin release are slightly delayed compared with insulin and antisynchronous to glucagon
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2007 (English)In: Regulatory Peptides, ISSN 0167-0115, E-ISSN 1873-1686, Vol. 144, no 1-3, 43-49 p.Article in journal (Refereed) Published
Abstract [en]

It was early proposed that somatostatin-producing delta-cells in pancreatic islets have local inhibitory effects on the release of insulin and glucagon. Recent observations that pulses of insulin and glucagon are antisynchronous make it important to examine the temporal characteristics of glucose-induced somatostatin release. Analysis of 30 s fractions from the perfused rat pancreas indicated that increase of glucose from 3 to 20 mmol/l results in initial suppression of somatostatin release followed by regular 4-5 min pulses. During continued exposure to 20 mmol/l glucose, the pulses of somatostatin overlapped those of insulin with a delay of 30 s. Somatostatin and glucagon pulses were coupled in antisynchronous fashion (phase shift 2.4 +/- 0.2 min), supporting the idea that the delta-cells have a local inhibitory effect on glucagon release. It was possible to remove the pulses of somatostatin and glucagon with maintenance of the insulin rhythmicity by addition of I mu mol/l of the P2Y(1) receptor antagonist MRS 2179.

Place, publisher, year, edition, pages
2007. Vol. 144, no 1-3, 43-49 p.
Keyword [en]
somatostatin pulse, MRS 2179, pancreas perfusion, purinoceptor
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-14959DOI: 10.1016/j.regpep.2007.06.003ISI: 000251601800007PubMedID: 17628719OAI: oai:DiVA.org:uu-14959DiVA: diva2:42730
Available from: 2008-02-01 Created: 2008-02-01 Last updated: 2017-12-11Bibliographically approved

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