{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T04:12:15Z","timestamp":1790655135998,"version":"4.1.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2008,5]]},"abstract":"\n The development of diabetes associated with stress, obesity, and metabolic syndrome involves elevated plasma glucocorticoid levels. It has been shown that short-term (<1 day) exposure to glucocorticoids reduces insulin secretion from pancreatic islets by affecting several steps of glucose signaling in \u03b2-cells. However, longer term direct effects of glucocorticoids on \u03b2-cells remain to be established. In this study, single \u03b2-cells isolated from rat islets were treated with glucocorticoids, mineralocorticoids, and their receptor agonists\/antagonists for 3 days in culture, followed by assessment of the \u03b2-cell responsiveness to glucose by measuring cytosolic Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n concentration ([Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n ) using fura-2. Following treatment with corticosterone at 10\u2013500\u200ang\/ml for 3 days, the first-phase [Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n response to 8.3\u200amM glucose in \u03b2-cells was suppressed. Simultaneous administration of RU-486, a glucocorticoid receptor (GR) antagonist, prevented this suppression. RU-486 by itself promoted the \u03b2-cell [Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n response to glucose. Conversely, dexamethasone (1000\u200ang\/ml), a highly selective GR agonist, impaired \u03b2-cell [Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n responses to glucose. A mineralocorticoid receptor (MR) antagonist spironolactone, co-administered with corticosterone, further depressed [Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n responses to glucose, while an MR ligand aldosterone attenuated the corticosterone inhibition of [Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n responses. Neither spironolactone nor aldosterone by itself affected [Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n responses. These results indicate that long-term treatment with corticosterone impairs \u03b2-cell [Ca\n 2<\/jats:sup>\n +<\/jats:sup>\n ]\n i<\/jats:sub>\n responses to glucose. This effect is mediated by GR and attenuated partially by simultaneous MR stimulation by corticosterone. The results show a novel function of MR to protect islet \u03b2-cells against deteriorating glucocorticoid action via GR.\n <\/jats:p>","DOI":"10.1677\/joe-07-0462","type":"journal-article","created":{"date-parts":[[2008,4,23]],"date-time":"2008-04-23T03:47:56Z","timestamp":1208922476000},"page":"221-229","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":21,"title":["Sub-chronic stimulation of glucocorticoid receptor impairs and mineralocorticoid receptor protects cytosolic Ca2+ responses to glucose in pancreatic \u03b2-cells"],"prefix":"10.1530","volume":"197","author":[{"given":"Masaru","family":"Koizumi","sequence":"first","affiliation":[{"name":"1Division of Integrative PhysiologyDepartment of Physiology2Department of SurgeryJichi Medical University School of Medicine, Yakushiji 3311-1, Shimotsuke, Tochigi 329-0498, Japan"},{"name":"1Division of Integrative PhysiologyDepartment of Physiology2Department of SurgeryJichi Medical University School of Medicine, Yakushiji 3311-1, Shimotsuke, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshihiko","family":"Yada","sequence":"additional","affiliation":[{"name":"1Division of Integrative PhysiologyDepartment of Physiology2Department of SurgeryJichi Medical University School of Medicine, Yakushiji 3311-1, Shimotsuke, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/joe.bioscientifica.com\/view\/journals\/joe\/197\/2\/221.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/joe.bioscientifica.com\/downloadpdf\/journals\/joe\/197\/2\/221.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:53:26Z","timestamp":1784555606000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/joe\/article\/197\/2\/221-229\/21705"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2008,3,4]]},"references-count":0,"journal-issue":{"issue":"2"},"URL":"https:\/\/doi.org\/10.1677\/joe-07-0462","relation":{},"ISSN":["0022-0795","1479-6805"],"issn-type":[{"value":"0022-0795","type":"print"},{"value":"1479-6805","type":"electronic"}],"subject":[],"published":{"date-parts":[[2008,3,4]]}}}