pubmed-article:1400388 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0521449 | lld:lifeskim |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0086045 | lld:lifeskim |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0025251 | lld:lifeskim |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0013790 | lld:lifeskim |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
pubmed-article:1400388 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:1400388 | pubmed:issue | 29 | lld:pubmed |
pubmed-article:1400388 | pubmed:dateCreated | 1992-11-18 | lld:pubmed |
pubmed-article:1400388 | pubmed:abstractText | Glucose stimulation of insulin release involves metabolism of the sugar and elevation of cytoplasmic calcium (Ca2+i) in pancreatic B-cells. We compared the dynamic changes of metabolism (fluorescence of endogenous reduced pyridine nucleotides, NAD(P)H), membrane potential (intracellular microelectrodes), and Ca2+i (fura-2 technique), in intact mouse islets. Glucose (15 mM) sequentially triggered an increase in NAD(P)H fluorescence, a depolarization with electrical activity, and a rise in Ca2+i. The change in NAD(P)H was monophasic and regular, whereas the changes in membrane potential and Ca2+i were multiphasic, with steady-state regular oscillations of similar average frequencies (about 2.2/min). Digital image analysis revealed that Ca2+i oscillations were synchronous in all regions of the islets. Omission of extracellular Ca2+ abolished the rise in Ca2+i but not the increase in NAD(P)H. Both electrical and Ca2+i oscillations disappeared in low external Ca2+ (1 mM), and became larger but slower in high Ca2+ (10 mM). Sustained depolarization (by tolbutamide, arginine, or high K+) and hyperpolarization (by diazoxide) of B-cells caused sustained increases and decreases of Ca2+i, respectively. In conclusion, the changes in membrane potential induced by various secretagogues trigger synchronous changes in Ca2+i in all B-cells of the islets. The oscillatory pattern of the electrical and Ca2+i responses induced by glucose is not accompanied by and thus probably not due to similar oscillations of metabolism. | lld:pubmed |
pubmed-article:1400388 | pubmed:language | eng | lld:pubmed |
pubmed-article:1400388 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1400388 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1400388 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1400388 | pubmed:month | Oct | lld:pubmed |
pubmed-article:1400388 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:1400388 | pubmed:author | pubmed-author:HenquinJ CJC | lld:pubmed |
pubmed-article:1400388 | pubmed:author | pubmed-author:GilonPP | lld:pubmed |
pubmed-article:1400388 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1400388 | pubmed:day | 15 | lld:pubmed |
pubmed-article:1400388 | pubmed:volume | 267 | lld:pubmed |
pubmed-article:1400388 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1400388 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1400388 | pubmed:pagination | 20713-20 | lld:pubmed |
pubmed-article:1400388 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:1400388 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1400388 | pubmed:articleTitle | Influence of membrane potential changes on cytoplasmic Ca2+ concentration in an electrically excitable cell, the insulin-secreting pancreatic B-cell. | lld:pubmed |
pubmed-article:1400388 | pubmed:affiliation | Unité de Diabétologie et Nutrition, University of Louvain Faculty of Medicine, Brussels, Belgium. | lld:pubmed |
pubmed-article:1400388 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1400388 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:1400388 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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