Potassium permeability of fetal rat pancreatic islets: abnormal sensitivity to glucose

Potassium channels of fetal rat islets have been recently reported to be inadequately regulated by stimulation with glucose when compared to islets of adult rats. Though in patch clamp experiments the properties of their KATP-channels were shown to be comparable to those from adult rats, until now no closure could be demonstrated with the technique measuring the 86Rb+ efflux. Using this technique, in the presence of a basal (3 mM) glucose concentration the 86Rb+ efflux was completely insensitive to a stimulation with glucose (5.6 mM) or tolbutamide. In contrast, in islets perifused in the absence of glucose the introduction of a low glucose concentration (3 mM) or stimulation with tolbutamide alone inhibited the 86Rb+ efflux, confirming the presence of functioning KATP-channels. The absolute value of the 86Rb+ efflux rate in the absence of glucose was, however, much lower in fetal rat islets as normally observed in adult rat islets. Apart from this, the ATP content of fetal rat islets remained unchanged at either glucose concentration tested. It is suggested that in islets of fetal rats a K+ permeability is present and can be inhibited by glucose and tolbutamide but in contrast to islets of adult rats the K+ efflux is already maximally inhibited in the presence of 3 mM glucose. This may be one reason why pancreatic islets of fetal rats do not respond to glucose-stimulation with an adequate calcium uptake and insulin release.