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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1993-2-17
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pubmed:abstractText |
1. Intracellular calcium [Ca2+]i and channel activity were simultaneously recorded in single, dissociated mouse beta-cells kept in culture for 1-3 days. [Ca2+]i was estimated from microfluorometric ratio methods using Indo-1. Channel activity was measured using the cell-attached configuration of the patch-clamp technique. 2. At low glucose concentrations (0.3 mM), resting K+ATP channel activity was prevalent. Increasing glucose up to 16 mM, produced a gradual decrease in K+ATP channel activity over a time course of 90-120 s (temperature = 23 degrees C) and an increase in [Ca2+]i. 3. In the majority of experiments, glucose elicited biphasic action currents (action potentials) which preceded the rise in [Ca2+]i. There was a close correlation between spike frequency and the levels of [Ca2+]i. 4. The sulphonylurea tolbutamide (1 mM) blocked K+ATP channels in 10-20 s. K+ATP channel blockade was associated with a quick rise in [Ca2+]i. 5. When K+ATP channel activity was stimulated in the presence of diazoxide (100 microM), increasing the glucose concentration from 3 to 16 mM produced a decrease in [Ca2+]i. Only when diazoxide was removed did glucose produce an increase in [Ca2+]i. 6. In a small population of cells, glucose (16 mM) produced a small decrease in K+ATP channel activity but not an increase in [Ca2+]i. In such cells, tolbutamide blocked K+ATP channels and produced an increase in [Ca2+]i. 7. These results demonstrate a close correlation between K+ATP channel activity and [Ca2+]i in beta-cells. The findings are consistent with the model in which glucose metabolism produces a rise in [Ca2+]i through the blockade of K+ATP channels, membrane depolarization and calcium current activation.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-1713562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-1876486,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2015391,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2129231,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2203530,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2403930,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2407553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2427706,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2431383,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2447283,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2458459,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2484976,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2497930,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2600854,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2689228,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2721487,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2825225,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-2855352,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-3146398,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-3276310,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-3281934,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-3510882,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-353252,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-3541896,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-3838314,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-4873864,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-6090930,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-6093775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-6095103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-6270629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-6296371,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-7035468,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1484353-785280
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
455
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
173-86
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pubmed:dateRevised |
2010-9-7
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pubmed:meshHeading |
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pubmed:year |
1992
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pubmed:articleTitle |
The relationship between glucose-induced K+ATP channel closure and the rise in [Ca2+]i in single mouse pancreatic beta-cells.
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pubmed:affiliation |
Department of Physiology, School of Medicine, University of Alicante, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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