Linked Life Data

17389589

Source:http://linkedlifedata.com/resource/pubmed/id/17389589

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
20
pubmed:dateCreated
2007-5-14
pubmed:abstractText
A current model ascribes glucose-induced insulin secretion to the interaction of a triggering pathway (K(ATP) channel-dependent Ca(2+) influx and rise in cytosolic [Ca(2+)](c)) and an amplifying pathway (K(ATP) channel-independent augmentation of secretion without further increase of [Ca(2+)](c)). However, several studies of sulfonylurea receptor 1 null mice (Sur1KO) failed to measure significant effects of glucose in their islets lacking K(ATP) channels. We addressed this issue that challenges the model. Compared with controls, fresh Sur1KO islets showed slightly elevated basal [Ca(2+)](c) and insulin secretion. In 15 mm glucose, the absolute rate of secretion was approximately 3-fold lower in Sur1KO than control islets, with only poor increase above base line. Overnight culture of Sur1KO islets in 10 mm glucose (not in 5 mm) augmented basal insulin secretion and considerably improved the response to 15 mm glucose, which reached higher values than in control islets, in which culture had little impact. Glucose stimulation during KCl depolarization showed that the amplifying pathway is functional in fresh and cultured Sur1KO islets. The differences in insulin secretion between fresh and cultured Sur1KO islets and between Sur1KO and control islets were not attributable to differences in insulin content, glucose oxidation rate, or synchronization of [Ca(2+)](c) oscillations. The unmasking of glucose-induced insulin secretion in beta-cells lacking K(ATP) channels is paradoxically due to improvement in the production of a triggering signal (elevated [Ca(2+)](c)). The results show that K(ATP) channels are not the only transducer of glucose effects on [Ca(2+)](c) in beta-cells. They explain controversies in the literature and refute arguments raised against the model implicating an amplifying pathway in glucose-induced insulin secretion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
282
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
14768-76
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:17389589-ATP-Binding Cassette Transporters, pubmed-meshheading:17389589-Adenosine Triphosphate, pubmed-meshheading:17389589-Animals, pubmed-meshheading:17389589-Calcium, pubmed-meshheading:17389589-Calcium Signaling, pubmed-meshheading:17389589-Cells, Cultured, pubmed-meshheading:17389589-Dose-Response Relationship, Drug, pubmed-meshheading:17389589-Glucose, pubmed-meshheading:17389589-Insulin, pubmed-meshheading:17389589-Islets of Langerhans, pubmed-meshheading:17389589-Mice, pubmed-meshheading:17389589-Mice, Knockout, pubmed-meshheading:17389589-Models, Biological, pubmed-meshheading:17389589-Multidrug Resistance-Associated Proteins, pubmed-meshheading:17389589-Potassium Channels, pubmed-meshheading:17389589-Potassium Channels, Inwardly Rectifying, pubmed-meshheading:17389589-Receptors, Drug, pubmed-meshheading:17389589-Sweetening Agents, pubmed-meshheading:17389589-Time Factors
pubmed:year
2007
pubmed:articleTitle
Overnight culture unmasks glucose-induced insulin secretion in mouse islets lacking ATP-sensitive K+ channels by improving the triggering Ca2+ signal.
pubmed:affiliation
Unit of Endocrinology and Metabolism, University of Louvain Faculty of Medicine, UCL55.30, B-1200 Brussels, Belgium.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't