Effects of valinomycin on Rb+ fluxes, ATP content and insulin release in pancreatic islets.
Valinomycin, 0.5-500 nM, was tested for its effects on pancreatic islets microdissected fron non-inbred ob/ob-mice. Valinomycin decreased the islet accumulation Rb+ and the content of ATP in a dose-dependent manner; efflux of Rb+ from pre-loaded islets was not noticeably changed. Rb+ accumulation and ATP content correlated markedly; on the model of linear regression, less than 10% of the change Rb+ accumulation in valinomycin-treated islets was statistically attributable to factors other than ATP. Valinomycin did not cause a prompt inhibition of glucose-stimulated insulin release that could reflect hyperpolarization due to increased K+ permeability. The following conclusions are drawn: 1) The plasma membranes of beta-cells resemble those of neurons in having such a high ion permeability as to be relatively little influenced by valinomycin; 2) Islet accumulation of Rb+ is due to a vectorial catalyst in theplasma membrane rather than to uptake by mitochondria; 3) Rb+ accumulation in islets is ATP-dependent.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D051379:Mice; D011868:Radioisotopes; D012413:Rubidium / Q000378:metabolism*; D014634:Valinomycin / Q000494:pharmacology*
D007328:Insulin; D011868:Radioisotopes; D014634:Valinomycin; D000255:Adenosine Triphosphate; D012413:Rubidium