Aims/hyypothesis. A sulphonylurea receptor, SUR1, and an inward rectifier p
otassium channel, Kir6.2, reconstitute the ATP-sensitive K+ channel that me
diates glucose-induced insulin secretion in pancreatic beta cells. We repor
ted previously that Kir6.2 were localized at insulin-, glucagon-, and somat
ostatin-producing cells. In this new study we aimed to determine the distri
bution of SUR1 in rat pancreatic islets and to suggest the location of the
ATP-sensitive K+ channels in the islet.
Methods. Western blot analysis was carried out using two anti-SUR1 antibodi
es, which had been raised against different portions of rat SUR1. SUR1, Kir
6.2, and islet hormones were then localized by indirect immunofluorescence
staining of the cryosections of rat pancreas.
Results. In Western blot analysis, each of the anti-SUR1 antibodies detecte
d a band at 140 kDa, which is close to the predicted molecular weight of SU
R1, in the homogenate of isolated pancreatic islets. Double immunofluoresce
nce staining of cryosections showed that SUR1 occurred all over the islets,
and that SUR1 colocalized with insulin, glucagon, somatostatin, and pancre
atic polypeptide. Kir6.2 was also shown to be present in pancreatic polypep
tide cells.
Conclusion/interpretation. Together with our previously reported data, the
above findings indicate that K-ATP channels comprising SUR1 and Kir6.2 occu
r not only in beta cells but also in the alpha, delta, and pancreatic polyp
eptide cells of the pancreatic islets, suggesting that therapeutic sulphony
lureas could act on these cells directly.