Glucose-induced mobilisation of intracellular Ca2+ in depolarised pancreatic islets.
Perifused rat pancreatic islets, prelabelled with 45Ca, were exposed for 90 min to a medium containing 30 mM K+, 0.25 mM diazoxide and 0.5 mM EGTA, but deprived of CaCl2. Either verapamil (0.05 mM) or Cd2+ (0.05 mM) were also present in the perifusate. Under these conditions a rise in D-glucose concentrations from either 2.8 to 16.7 mM or zero to 8.3 mM increased both 45Ca outflow and insulin release, after an initial and transient decrease in effluent radioactivity. These findings suggest that, in islets depolarised by exposure to a high extracellular concentration of K+, D-glucose provokes an intracellular redistribution of Ca2+ ions and subsequent stimulation of insulin release. The functional response to D-glucose is apparently not attributable to either the closing of ATP-sensitive K+ channels, which were actually activated by diazoxide, or stimulation of Ca2+ influx, which was prevented by the absence of extracellular Ca2+. The present experimental design thus reveals a novel component of the glucose-induced remodelling of Ca2+ fluxes in islet cells. Such an effect might also be operative under physiological conditions, when the hexose leads to depolarisation of the islet B-cells.
Jijakli
H
H
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Malaisse
W J
WJ
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar
D007328:Insulin; D005947:Glucose; D002118:Calcium