Linked Life Data

16914887

Source:http://linkedlifedata.com/resource/pubmed/id/16914887

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2006-8-17
pubmed:abstractText
The metabolic coupling of insulin secretion by pancreatic beta cells is mediated by membrane depolarization due to increased glucose-driven ATP production and closure of K(ATP) channels. Alternative pathways may involve the activation of anion channels by cell swelling upon glucose uptake. In INS-1E insulinoma cells superfusion with an isotonic solution containing 20 mM glucose or a 30% hypotonic solution leads to the activation of a chloride conductance with biophysical and pharmacological properties of anion currents activated in many other cell types during regulatory volume decrease (RVD), i.e. outward rectification, inactivation at positive membrane potentials and block by anion channel inhibitors like NPPB, DIDS, 4-hydroxytamoxifen and extracellular ATP. The current is not inhibited by tolbutamide and remains activated for at least 10 min when reducing the extracellular glucose concentration from 20 mM to 5 mM, but inactivates back to control levels when cells are exposed to a 20% hypertonic extracellular solution containing 20 mM glucose. This chloride current can likewise be induced by 20 mM 3-Omethylglucose, which is taken up but not metabolized by the cells, suggesting that cellular sugar uptake is involved in current activation. Fluorescence resonance energy transfer (FRET) experiments show that chloride current activation by 20 mM glucose and glucose-induced cell swelling are accompanied by a significant, transient redistribution of the membrane associated fraction of ICln, a multifunctional 'connector hub' protein involved in cell volume regulation and generation of RVD currents.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1015-8987
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
21-34
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16914887-3-O-Methylglucose, pubmed-meshheading:16914887-Animals, pubmed-meshheading:16914887-Anions, pubmed-meshheading:16914887-Cell Line, Tumor, pubmed-meshheading:16914887-Cell Membrane, pubmed-meshheading:16914887-Cytosol, pubmed-meshheading:16914887-Fluorescence Resonance Energy Transfer, pubmed-meshheading:16914887-Glucose, pubmed-meshheading:16914887-Hypertonic Solutions, pubmed-meshheading:16914887-Hypoglycemic Agents, pubmed-meshheading:16914887-Hypotonic Solutions, pubmed-meshheading:16914887-Insulinoma, pubmed-meshheading:16914887-Ion Channels, pubmed-meshheading:16914887-Membrane Potentials, pubmed-meshheading:16914887-Patch-Clamp Techniques, pubmed-meshheading:16914887-Protein Transport, pubmed-meshheading:16914887-Rats, pubmed-meshheading:16914887-Tolbutamide
pubmed:year
2006
pubmed:articleTitle
Glucose induces anion conductance and cytosol-to-membrane transposition of ICln in INS-1E rat insulinoma cells.
pubmed:affiliation
Institute of Physiology and Pathophysiology, Paracelsus Private Medical University, Salzburg.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't