Disturbed fluxes of Rb+(K+) and Cl- in islets of spontaneously diabetic mice (C57BL/KsJ-db/db).
KsJ-db/db-mouse islets have a well functioning cation pump. Islets from diabetic mice did not accumulate less RB+ and did not exhibit less activity of K+-stimulated p-nitrophenyl phosphatase than did those of non-diabetic controls. In fact, the diabetic mouse islets accumulated Rb+ somewhat more effectively than normal mouse islets. This difference could be explained by the reduced Rb+ permeability in the islets cells of diabetic mice. The kinetics of Cl- efflux were also changed in the islets from diabetic mice, suggesting an increased Cl- permeability. These anomalous regulations can explain the defective membrane potential and the high basal release of insulin in diabetic mice. The D-glucose concentration had no effect on the permeabilities to Rb+ and Cl-. This is in contrast, to normal controls, in whose islets 20 mmol/l D-glucose decreases the Rb+ permeability and increases the Cl- permeability. This glucose insensitivity of ion permeabilities may help to explain the secretory unresponsiveness of KsJ-db/db-mouse beta-cells.
D000375:Aging; D000818:Animals; D001693:Biological Transport, Active; D002712:Chlorides / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D066298:In Vitro Techniques; D007515:Islets of Langerhans / Q000254:growth & development / Q000378:metabolism*; D007700:Kinetics; D051379:Mice; D008815:Mice, Inbred Strains; D011188:Potassium / Q000378:metabolism*; D012413:Rubidium / Q000378:metabolism*
D002712:Chlorides; D012413:Rubidium; D011188:Potassium