86Rb+ fluxes and K+-stimulated nitrophenyl phosphatase activity in the pancreatic islets of genetically diabetic mice (C57BL/KsJ-db/db).
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 activity 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.
D009597:4-Nitrophenylphosphatase / Q000378:metabolism*; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000378:metabolism*; D005260:Female; D066298:In Vitro Techniques; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D011868:Radioisotopes; D012413:Rubidium / Q000378:metabolism*
D011868:Radioisotopes; D010744:Phosphoric Monoester Hydrolases; D009597:4-Nitrophenylphosphatase; D012413:Rubidium; D011188:Potassium