{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:48:05Z","timestamp":1771627685815,"version":"3.50.1"},"reference-count":0,"publisher":"American Diabetes Association","issue":"11","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1983,11,1]]},"abstract":"<jats:p>Islet culture at a low glucose concentration results in a progressive impairment of glucose-induced insulin release. The role of Ca2+ in this defect was studied by comparing rat islets cultured for 6 days either at 8.3 mM (control) or 2.8 mM glucose. For measurement of 45Ca content and 45Ca2+ efflux, islets were kept in the presence of 45Ca2+ throughout. In islets cultured at 8.3 mM glucose, stimulation with 16.7 mM glucose during perifusion caused a typical biphasic pattern of insulin release paralleled by an increase in the rate of 45Ca2+ efflux. Both effects of glucose were markedly reduced in islets kept at 2.8 mM glucose, despite a similar insulin content. Islet 45Ca content was reduced. Both 45Ca content and insulin release were restored when islets were kept for an additional 24 h at 8.3 mM glucose. Insulin release induced by 3-isobutyl-1-methylxanthine (IBMX) or \u03b1-ketoisocaproic acid was not impaired, demonstrating that there is no generalized release defect. In contrast, glyceraldehyde- or K+-induced release was decreased. In islets maintained at 2.8 mM glucose, the stimulatory effect of glucose on Ca2+ uptake and the inhibitory effect on Ca2+ efflux (in the absence of Ca2+) were found to be operative. A defect may therefore lie distal to the Ca2+ uptake step involving either the mechanism by which glucose uses cellular Ca or another step yet to be identified.<\/jats:p>","DOI":"10.2337\/diab.32.11.993","type":"journal-article","created":{"date-parts":[[2013,9,19]],"date-time":"2013-09-19T17:16:02Z","timestamp":1379610962000},"page":"993-1000","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":12,"title":["Involvement of Ca2+ in the Impaired Glucose-induced Insulin Release from Islets Cultured at Low Glucose"],"prefix":"10.2337","volume":"32","author":[{"given":"Eberhard G","family":"Siegel","sequence":"first","affiliation":[{"name":"Institut de Biochimie Clinique, University of Geneva\u2008Geneva, Switzerland\u2008Department of Gastroenterology and Metabolism, University of G\u00f6ttingen, G\u00f6ttingen\u2008Federal Republic of Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Claes B","family":"Wollheim","sequence":"additional","affiliation":[{"name":"Institut de Biochimie Clinique, University of Geneva\u2008Geneva, Switzerland\u2008Department of Gastroenterology and Metabolism, University of G\u00f6ttingen, G\u00f6ttingen\u2008Federal Republic of Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Danilo","family":"Janjic","sequence":"additional","affiliation":[{"name":"Institut de Biochimie Clinique, University of Geneva\u2008Geneva, Switzerland\u2008Department of Gastroenterology and Metabolism, University of G\u00f6ttingen, G\u00f6ttingen\u2008Federal Republic of Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G\u00e9rard","family":"Ribes","sequence":"additional","affiliation":[{"name":"Institut de Biochimie Clinique, University of Geneva\u2008Geneva, Switzerland\u2008Department of Gastroenterology and Metabolism, University of G\u00f6ttingen, G\u00f6ttingen\u2008Federal Republic of Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Geoffrey W G","family":"Sharp","sequence":"additional","affiliation":[{"name":"Institut de Biochimie Clinique, University of Geneva\u2008Geneva, Switzerland\u2008Department of Gastroenterology and Metabolism, University of G\u00f6ttingen, G\u00f6ttingen\u2008Federal Republic of Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1167","container-title":["Diabetes"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.org\/diabetes\/diabetes\/article-pdf\/32\/11\/993\/352446\/32-11-993.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article-pdf\/32\/11\/993\/352446\/32-11-993.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,11,2]],"date-time":"2022-11-02T16:39:27Z","timestamp":1667407167000},"score":1,"resource":{"primary":{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article\/32\/11\/993\/5686\/Involvement-of-Ca2-in-the-Impaired-Glucose-induced"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1983,11,1]]},"references-count":0,"journal-issue":{"issue":"11","published-print":{"date-parts":[[1983,11,1]]}},"URL":"https:\/\/doi.org\/10.2337\/diab.32.11.993","relation":{},"ISSN":["0012-1797","1939-327X"],"issn-type":[{"value":"0012-1797","type":"print"},{"value":"1939-327X","type":"electronic"}],"subject":[],"published":{"date-parts":[[1983,11,1]]}}}