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Protein kinase C activity affects glucose-induced oscillations in cytoplasmic free Ca2+ in the pancreatic B-cell.
Authors:H Kindmark  M K?hler  S Efendi?  P Rorsman  O Larsson  P O Berggren
Affiliation:Rolf Luft Center for Diabetes Research, Department of Endocrinilogy, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
Abstract:Acute stimulation of protein kinase C (PKC) inhibited glucose-induced slow oscillations in cytoplasmic free Ca(2+)-concentration, [Ca2+]i, in mouse pancreatic B-cells. In PKC-depleted cells glucose induced rapid transients in [Ca2+]i, lasting for approximately 10 s, superimposed on the slow oscillations in [Ca2+]i. It was demonstrated that the transients did not occur in the absence of extracellular Ca2+. Each transient typically was preceded by a slow increase in [Ca2+]i, representing the rising phase of an ordinary glucose-induced slow oscillation, and the [Ca2+]i, immediately after a transient was lower than just before the spike. These data further emphasize the interplay between voltage-dependent Ca(2+)-channels and the phospholipase C system in the regulation of B-cell [Ca2+]i-oscillations.
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