Depolarizing stimuli reduce Ca(2+)/calmodulin-dependent protein kinase II activity in islets of Langerhans

Elevations in intracellular Ca(2+) ([Ca(2+)](i)) initiate insulin secretion from pancreatic beta-cells, but the secretory responses become rapidly desensitised to maintained elevations in [Ca(2+)](i). We have investigated the mechanisms underlying the Ca(2+) desensitization of insulin secretion usin...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2000-04, Vol.270 (3), p.1119-1123
Main Authors: Harris, T E, Persaud, S J, Squires, P E, Jones, P M
Format: Article
Language:English
Subjects:
Animals
Calcium - pharmacology
Calcium - physiology
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Cell Membrane Permeability
Electrophysiology
Glucose - pharmacology
In Vitro Techniques
Insulin - metabolism
Insulin Secretion
Islets of Langerhans - drug effects
Islets of Langerhans - enzymology
Islets of Langerhans - physiology
Membrane Potentials
Potassium Chloride - pharmacology
Rats
Tolbutamide - pharmacology
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Summary:Elevations in intracellular Ca(2+) ([Ca(2+)](i)) initiate insulin secretion from pancreatic beta-cells, but the secretory responses become rapidly desensitised to maintained elevations in [Ca(2+)](i). We have investigated the mechanisms underlying the Ca(2+) desensitization of insulin secretion using electrically permeabilized rat islets of Langerhans. Measurements of Ca(2+)/calmodulin-dependent protein kinase II (CaMK II) enzyme activity and immunoreactivity in permeabilized islets demonstrated Ca(2+)-induced reductions in enzyme activity which could not be attributed to reductions in CaMK II immunoreactive protein. Measurements in intact islets demonstrated that the Ca(2+)-induced reduction of CaMK II activity was also operative in intact cells, suggesting that this mechanism may have pathophysiological implications for beta-cell function.
ISSN:0006-291X
DOI:10.1006/bbrc.2000.2563