Modifications of the pancreatic beta-cell function after lowering their potassium content.
beta-cell-rich pancreatic islets from ob/ob-mice were kept for 3 days in a culture medium and analysed for their content of potassium. In a normal ionic milieu intracellular potassium was calculated as 190-260 mM. Whereas this concentration remained essentially unaffected after lowering extracellular K+ to 1.5 mM, further reduction to 0.15 mM depressed islet potassium to 5% or less of its original value. Irrespective of its medium concentration, potassium in the islets increased when glucose was raised from 1 to 20 mM. Depression of the islet potassium was associated with a rise of intracellular calcium. Despite profound depletion of potassium, the beta-cells maintained their insulin content and could still oxidize glucose at a substantial rate. When potassium was suppressed to 25% or less of the original content, the beta-cells responded to glucose with a paradoxical inhibition of insulin release. After 3 days of potassium depletion, exposure to a normal ionic milieu neither restored the intracellular content of potassium nor a stimulated insulin secretory response to glucose.
D000818:Animals; D002118:Calcium / Q000032:analysis; D002478:Cells, Cultured; D005110:Extracellular Space / Q000032:analysis; D005947:Glucose / Q000378:metabolism; D007328:Insulin / Q000032:analysis; D007515:Islets of Langerhans / Q000032:analysis*; D051379:Mice; D008820:Mice, Obese; D010084:Oxidation-Reduction; D011188:Potassium / Q000032:analysis*
D007328:Insulin; D005947:Glucose; D011188:Potassium; D002118:Calcium