Protein kinase C activity affects glucose-induced oscillations in cytoplasmic free Ca2+ in the pancreatic B-cell.
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.
Kindmark
H
H
Rolf Luft Center for Diabetes Research, Department of Endocrinilogy, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
Köhler
M
M
Efendić
S
S
Rorsman
P
P
Larsson
O
O
Berggren
P O
PO
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002413:Cations, Divalent; D004789:Enzyme Activation; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000166:cytology / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D051379:Mice; D011493:Protein Kinase C / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D002413:Cations, Divalent; D011493:Protein Kinase C; D005947:Glucose; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium