Summary
Fluxes of 86Rb+ and hydrolysis of p-nitrophenyl phosphate were measured in collagenase-isolated islets of diabetic C57BL/KsJ-db/db-mice and normal controls (C57BL/KsJ-+/+). Both types of islets accumulated Rb+ avidly, as originally reported for hand-dissected islets of non-inbred ob/ ob-mice. KsJ-db/db-mouse islets showed enhanced accumulation of Rb+ and normal acitivity of K+-activated nitrophenyl phosphatase. D-glucose, 20 mmol/l, inhibited Rb+ efflux in normal islets but not in those from KsJ-db/db-mice. The glucose insensitivity of Rb+ efflux was observed in young animals, which exhibit glucose-induced insulin release, as well as in old animals, which do not secrete insulin in response to glucose. The anomalous regulation of Rb+ efflux already present in young animals may bear on the liability of KsJ-db/db-mouse B-cells to develop defective control of membrane potential, an abnormal metabolism of cyclic AMP, and a marked failure of insulin secretory capacity.
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Berglund, O., Sehlin, J. & Täljedal, I.B. 86Rb+ fluxes and K+-stimulated nitrophenyl phosphatase acitvity in the pancreatic islets of genetically diabetic mice (C57BL/KsJ-db/db). Diabetologia 15, 191–195 (1978). https://doi.org/10.1007/BF00421238
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DOI: https://doi.org/10.1007/BF00421238