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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1993-9-16
|
| pubmed:abstractText |
Although closure of the ATP-sensitive K+ (K+ ATP) channel produced by glucose metabolism in the B-cell has been considered mediating the major signal for glucose-induced insulin release, evidences indicating the existence of the K+ ATP channel-independent, insulinotropic action of glucose have recently been accumulated. Namely, glucose stimulates insulin release by the B-cell with a full inhibition of the K+ ATP channel closure by diazoxide, a K+ ATP channel opener, provided cytosolic calcium is elevated. Glucose clearly elicits insulin release even if the K+ ATP channel is maximally inhibited by high concentration of sulfonylurea. In this case, glucose-induced insulin release is associated with net increase, not decrease, of K+ outflow, indicating glucose is opening K+ channels. Thus, closure of the K+ ATP channel is highly unlikely to be the mechanism responsible for the insulinotropic action of glucose under these conditions. The K+ ATP channel-independent glucose action is dependent upon physiological glucose concentration (2-30 mM) and the degree of cytosolic calcium elevation. The K+ ATP channel-independent, glucose-induced insulin release shows gradually increasing monophasic pattern which temporally resembles the second phase response of glucose-induced insulin release. The role of glucose metabolism in the K+ ATP channel-independent glucose action remains to be established. Glucose action at the B-cell can now be subdivided into two classes: one is the K+ ATP channel-dependent and the other is the K+ ATP channel-independent. The two branches may be mutually interrelated to cause normal, biphasic insulin secretion.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
1210-0668
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
26
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
159-62
|
| pubmed:dateRevised |
2011-11-17
|
| pubmed:meshHeading | |
| pubmed:year |
1992
|
| pubmed:articleTitle |
ATP-sensitive K+ channel-independent, insulinotropic action of glucose in the B-cells.
|
| pubmed:affiliation |
Department of Geriatrics, Endocrinology and Metabolism, Shinshu University School of Medicine, Matsumoto, Japan.
|
| pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
|