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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1987-9-30
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pubmed:abstractText |
The diminished insulin secretion of type 2 diabetes might result from abnormal regulation of the potassium permeability which leads to beta-cell depolarization. The possibility of a generalized defect has been investigated in vitro by the stimulation of 86Rb efflux from red cells of type 2 diabetic patients by calcium ionophore and its inhibition by quinine. Diabetic subjects and control subjects had identical 86Rb efflux stimulated by 0.2-0.6 microM calcium ionophore A23187 and identical inhibition by quinine with mean Ki 6 microM and 4 microM quinine respectively for 0.2 microM ionophore and mean Ki 38 microM and 37 microM quinine respectively for 0.6 microM ionophore.
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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 |
May
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pubmed:issn |
0265-5985
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
19-21
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pubmed:dateRevised |
2007-9-11
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pubmed:meshHeading |
pubmed-meshheading:2441919-Adult,
pubmed-meshheading:2441919-Calcimycin,
pubmed-meshheading:2441919-Calcium,
pubmed-meshheading:2441919-Diabetes Mellitus, Type 2,
pubmed-meshheading:2441919-Erythrocytes,
pubmed-meshheading:2441919-Humans,
pubmed-meshheading:2441919-Ion Channels,
pubmed-meshheading:2441919-Middle Aged,
pubmed-meshheading:2441919-Potassium,
pubmed-meshheading:2441919-Quinine
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pubmed:year |
1987
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pubmed:articleTitle |
Normal calcium-activated potassium channel in red cells in type 2 diabetes.
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pubmed:publicationType |
Journal Article
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