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1 Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512, Japan
2 Department of Physiology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan
The present study was conducted to evaluate the role of conventional protein kinase C (PKC) in calcium-evoked insulin secretion. In rat ß cells transfected with green fluorescent protein-tagged PKC-
(PKC-–EGFP), a depolarizing concentration of potassium induced transient elevation of cytoplasmic free calcium ([Ca2+]c), which was accompanied by transient translocation of PKC-–EGFP from the cytosol to the plasma membrane. Potassium also induced transient translocation of PKC-
–EGFP, the C1 domain of PKC-
and PKC-
–GFP. A high concentration of glucose induced repetitive elevation of [Ca2+]c and repetitive translocation of PKC-–EGFP. Diazoxide completely blocked both elevation of [Ca2+]c and translocation of PKC-–EGFP. We then studied the role of conventional PKC in calcium-evoked insulin secretion using rat islets. When islets were incubated for 10 min with high potassium, Gö-6976, an inhibitor of conventional PKC, and PKC- pseudosubstrate fused to antennapedia peptide (Antp-PKC19–31) increased potassium induced secretion. Similarly, insulin release induced by high glucose for 10 min was enhanced by Gö-6976 and Antp-PKC19–31. However, when islets were stimulated for 60 min with high glucose, both Gö-6976 and Antp-PKC19–31 reduced glucose-induced insulin secretion. Similar results were obtained by transfection of dominant-negative PKC- using adenovirus vector. Taken together, PKC- is activated when cells are depolarized by a high concentration of potassium or glucose. Conventional PKC is inhibitory on depolarization-induced insulin secretion per se, but it also augments glucose-induced secretion.
(Received 5 July 2004;
accepted after revision 17 September 2004;
first published online 23 September 2004)
Corresponding author I. Kojima: Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512, Japan. Email: ikojima{at}showa.gunma-u.ac.jp
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