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.