Insulin secretion

dc.contributor.authorGheibi, Sevda
dc.contributor.authorGhasemi, Asghar
dc.date.accessioned2020-12-17T12:16:35Z
dc.date.available2020-12-17T12:16:35Z
dc.date.issued2020-09-08
dc.description.abstractNitric oxide (NO) is a gas that serves as a ubiquitous signaling molecule participating in physiological activities of various organ systems. Nitric oxide is produced in the endocrine pancreas and contributes to synthesis and secretion of insulin. The potential role of NO in insulin secretion is disputable – both stimulatory and inhibitory effects have been reported. Available data indicate that effects of NO critically depend on its concentration. Different isoforms of NO synthase (NOS) control this and have the potential to decrease or increase insulin secretion. In this review, the role of NO in insulin secretion as well as the possible reasons for discrepant findings are discussed. A better understanding of the role of NO system in the regulation of insulin secretion may facilitate the development of new therapeutic strategies in the management of diabetes.en
dc.identifier.citationGheibi, S., & Ghasemi, A. (2020). Insulin secretion: The nitric oxide controversy . EXCLI Journal, 19, 1227-1245. https://doi.org/10.17179/excli2020-2711en
dc.identifier.issn1611-2156
dc.identifier.urihttp://hdl.handle.net/2003/39916
dc.identifier.urihttp://dx.doi.org/10.17877/DE290R-21806
dc.language.isoen
dc.publisherIfADo - Leibniz Research Centre for Working Environment and Human Factors, Dortmunden
dc.relation.ispartofseriesEXCLI Journal;Vol. 19 2020
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectNitric oxideen
dc.subjectInsulin secretionen
dc.subjectInsulin synthesisen
dc.subject.ddc610
dc.titleInsulin secretionen
dc.title.alternativethe nitric oxide controversyen
dc.typeText
dc.type.publicationtypearticle
dcterms.accessRightsopen access
eldorado.dnb.deposittruede
eldorado.dnb.zdberstkatid2132560-1
eldorado.dnb.zdberstkatidtrue
eldorado.identifier.urlhttps://www.excli.de/index.php/excli/article/view/2711

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