Linked Life Data

8900404

Source:http://linkedlifedata.com/resource/pubmed/id/8900404

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-12-16
pubmed:abstractText
Glucose was found to induce large amplitude oscillations of cytoplasmic Sr2+ and Ca2+ in individual pancreatic beta-cells exposed to the respective cation. Subsequent addition of 20 nM glucagon or other agents raising cAMP triggered pronounced transients superimposed upon the large amplitude oscillations. Hyperpolarization with diazoxide prevented both the large amplitude oscillations and the superimposed transients. After short exposure to carbachol or ATP there was a temporary, and after addition of the Ca2+-ATPase inhibitor thapsigargin a permanent, disappearance of the transients with persistence of the glucose-induced large amplitude oscillations. The Ca2+ channel blocker methoxyverapamil exhibited opposite specificity in preventing the large amplitude oscillations under conditions when the transients often remained. In the presence of methoxyverapamil the transients disappeared during diazoxide hyperpolarization and were restored by subsequent K+ depolarization, which also elevated the content of inositol 1,4,5-trisphosphate (IP3) by 45%. The glucagon-induced transients were obliterated by 12-O-tetradecanoylphorbol 13-acetate, insensitive to ryanodine and paradoxically inhibited by high concentrations of caffeine. The IP3-mediated intracellular ion mobilization induced by carbachol was amplified by glucagon. The results indicate that depolarization-dependent formation of IP3 causes intracellular Ca2+ mobilization in individual beta-cells when the IP3 receptors are sensitized by cAMP. This mechanism may be an important determinant for the electrophysiological burst activity in intact pancreatic islets due to the presence of endogenous glucagon.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0003-9861
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
334
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
295-302
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8900404-Animals, pubmed-meshheading:8900404-Caffeine, pubmed-meshheading:8900404-Calcium, pubmed-meshheading:8900404-Cells, Cultured, pubmed-meshheading:8900404-Cyclic AMP, pubmed-meshheading:8900404-Cytosol, pubmed-meshheading:8900404-Diazoxide, pubmed-meshheading:8900404-Gallopamil, pubmed-meshheading:8900404-Glucagon, pubmed-meshheading:8900404-Glucose, pubmed-meshheading:8900404-Inositol 1,4,5-Trisphosphate, pubmed-meshheading:8900404-Islets of Langerhans, pubmed-meshheading:8900404-Kinetics, pubmed-meshheading:8900404-Membrane Potentials, pubmed-meshheading:8900404-Mice, pubmed-meshheading:8900404-Mice, Obese, pubmed-meshheading:8900404-Oscillometry, pubmed-meshheading:8900404-Potassium, pubmed-meshheading:8900404-Ryanodine, pubmed-meshheading:8900404-Signal Transduction, pubmed-meshheading:8900404-Strontium, pubmed-meshheading:8900404-Tetradecanoylphorbol Acetate
pubmed:year
1996
pubmed:articleTitle
Crosstalk between the cAMP and inositol trisphosphate-signalling pathways in pancreatic beta-cells.
pubmed:affiliation
Department of Medical Cell Biology, Uppsala University, Biomedicum, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't