Defective regulation of Cl- permeability in islets of diabetic mice [C57BL/KsJ(db/db)].
Efflux of 36Cl- from prelabeled, collagenase-isolated islets of noninbred ob/ob mice, inbred diabetic [C57BL/KsJ(db/db)] mice, and nondiabetic [C57BL/KsJ(+/+)] mice was studied by nonrecirculating perifusion. Islets of both ob/ob mice and nondiabetic KsJ mice showed similar rates of basal 36Cl- efflux, D-glucose stimulation of the 36Cl- efflux, and net uptake of 36Cl- at apparent isotope equilibrium. The 36Cl- efflux in islets from both young and old KsJ-db/db mice was almost insensitive to the D-glucose concentration. The basal rate of 36Cl- efflux in islets from young and old db/db mice was increased, indicating an abnormally high Cl- permeability. It is suggested that the defective regulation of the membrane potential in B-cells from [C57BL/KsJ(db/db)] mice may at least partly be caused by a db-mediated defect in the regulation of Cl- permeability.
D000375:Aging; D000818:Animals; D001692:Biological Transport; D002712:Chlorides / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D007515:Islets of Langerhans / Q000254:growth & development / Q000378:metabolism*; D051379:Mice; D008815:Mice, Inbred Strains; D008820:Mice, Obese; D010477:Perfusion; D010539:Permeability
D002712:Chlorides