%0 Journal Article
%T ATP-sensitive potassium channel (KATP channel) expression in the normal canine pancreas and in canine insulinomas
%A Vicky R Donley
%A Erin K Hiskett
%A Aimee C Kidder
%A Thomas Schermerhorn
%J BMC Veterinary Research
%D 2005
%I BioMed Central
%R 10.1186/1746-6148-1-8
%X Pancreatic tissue from normal dogs and tumor tissue from three dogs with histologically-confirmed insulinomas was examined for expression of KATP channel subunits (SUR1 and Kir6.2) using RT-PCR. Normal canine pancreas expressed SUR1 and Kir6.2 subunits of the KATP channel. The partial nucleotide sequences for SUR1 and Kir6.2 obtained from the normal pancreas showed a high degree of homology to published sequences for other mammalian species. SUR1 and Kir6.2 expression was observed in each of the three canine insulinomas examined. Comparison of short sequences from insulinomas with those obtained from normal pancreas did not reveal any mutations in either SUR1 or Kir6.2 in any of the insulinomas.Canine pancreatic KATP channels have the same subunit composition as those found in the endocrine pancreases of humans, rats, and mice, suggesting that the canine channel is regulated in a similar fashion as in other species. SUR1 and Kir6.2 expression was found in the three insulinomas examined indicating that unregulated insulin secretion by these tumors does not result from failure to express one or both KATP channel subunits.The ATP-sensitive potassium (KATP) channel is a crucial component of the pancreatic beta cell insulin secretion pathway and a target for drugs that modulate insulin secretion. In the endocrine cells of the pancreas, KATP channel is composed of two subunits: a sulfonylurea receptor (SUR 1), which contains two adenine nucleotide binding domains [1], and an inward rectifying potassium channel (Kir6.2), which conducts potassium ions [2]. The KATP channel is important for sensing the metabolic state of the pancreatic beta cell and initiating the changes in membrane potential that precede insulin exocytosis. In the presence of high concentrations of glucose, beta cell metabolism of the sugar increases ATP production. The resulting rise in the cellular ATP/ADP ratio causes closure of KATP channels, which bind ATP and ADP at different sites [3]. The decrease
%U http://www.biomedcentral.com/1746-6148/1/8