| pubmed-article:2472299 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2472299 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:2472299 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
| pubmed-article:2472299 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:2472299 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:2472299 | lifeskim:mentions | umls-concept:C1708373 | lld:lifeskim |
| pubmed-article:2472299 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:2472299 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:2472299 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:2472299 | pubmed:dateCreated | 1989-8-8 | lld:pubmed |
| pubmed-article:2472299 | pubmed:abstractText | With a glucose-responsive beta-cell line (HIT cells), we tested the hypothesis that the cytosolic free-Ca2+ level ([Ca2+]i) is an intracellular signal through which a rise in cyclic AMP (cAMP) levels is transmitted to potentiate glucose-stimulated insulin secretion. In these cells, glucose stimulates the acute release of insulin without increasing [Ca2+]i or altering cAMP content. Either forskolin or 3-isobutylmethylxanthine (IBMX) potentiated glucose-stimulated insulin secretion and increased cAMP levels. At either a submaximal glucose concentration or maximally stimulatory glucose concentration, both IBMX and forskolin triggered a rapid rise in [Ca2+]i (1.9- and 1.5-fold increase over basal levels, respectively). Similarly, glucagon stimulated a 1.3-fold increase in [Ca2+]i over basal levels. The effect on [Ca2+]i required glucose and was secondary to Ca2+ influx through voltage-dependent Ca2+ channels because it was blocked by either chelation of extracellular Ca2+ with EGTA or by the Ca2+-channel blockers verapamil and nimodipine. Verapamil also inhibited IBMX potentiation of glucose-stimulated insulin secretion and the IBMX-induced rise in [Ca2+]i in a dose-dependent manner with IC50s of 2 x 10(-5) and 4 x 10(-6) M, respectively. We conclude that in the beta-cell, a rise in cAMP levels increases Ca2+ influx through voltage-dependent Ca2+ channels and that this represents a mechanism by which cAMP potentiates glucose-stimulated insulin secretion in beta-cells. | lld:pubmed |
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| pubmed-article:2472299 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2472299 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:2472299 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2472299 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:2472299 | pubmed:issn | 0012-1797 | lld:pubmed |
| pubmed-article:2472299 | pubmed:author | pubmed-author:BallC ACA | lld:pubmed |
| pubmed-article:2472299 | pubmed:author | pubmed-author:HillR SRS | lld:pubmed |
| pubmed-article:2472299 | pubmed:author | pubmed-author:RajanA SAS | lld:pubmed |
| pubmed-article:2472299 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2472299 | pubmed:volume | 38 | lld:pubmed |
| pubmed-article:2472299 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2472299 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2472299 | pubmed:pagination | 874-80 | lld:pubmed |
| pubmed-article:2472299 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:2472299 | pubmed:meshHeading | pubmed-meshheading:2472299-... | lld:pubmed |
| pubmed-article:2472299 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2472299 | pubmed:articleTitle | Effect of rise in cAMP levels on Ca2+ influx through voltage-dependent Ca2+ channels in HIT cells. Second-messenger synarchy in beta-cells. | lld:pubmed |
| pubmed-article:2472299 | pubmed:affiliation | Department of Medicine, Baylor College of Medicine, Houston, TX 77030. | lld:pubmed |
| pubmed-article:2472299 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2472299 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2472299 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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