[Characteristics of hepatocyte rough endoplasmic reticulum single cationic channel in streptozocin-induced diabetic rats]

The role of ion channels and particularly cationic channels in the pathogenesis of various diseases are being considered carefully. The diabetes mellitus is a common disease which is initiated by ion channel disturbances. This study was done to determine the characteristics of hepatocyte rough endoplasmic reticulum single cationic channel in Streptozocin-induced diabetic rats. This experimental study was done on 10 male adult Wistar rats and animals were randomly allocaied into diabetic and control groups. Diabetes induced by STZ [65 mg/kg/bw] intraperitounally. Rough endoplasmic reticulum vesicles were extracted following rat liver excision, homogenization and ultracentrifuging. The bilayer membrane formation was prepared by painting phosphatidylcholine on 250 micro M aperture in between Cis and Trans sides. The RER vesicles incorporation was performed through gentle and delicate touch of membrane using a dentistry needle. The Pclamp9 software was used for ion channel activity characteristic analysis. The cationic channel current amplitude did not change significantly in voltages more than+3o mV but their open probability [Po] decreased in diabetic group [P<0.05]. More severe changes in channel activity were seen in potentials less than the reverse potential. In addition to significant increase of channel Po [P<0.05], also, the channel unitary currents were significantly decreased [P<0.05]. The mean current amplitude and channel open probability in voltage+40 mV were 17 +/- 2.14 pA and 0.68 +/- 0.01 in control group respectively, whereas, the values of these parameters reached to 18.5 +/- 2.5 and 0.26 +/- 0.03, respectively. In voltage-10 mV, the values of mean current amplitude and Po were-22.3 +/- 2.14 pA and<0.1 in control group, respectively but the values changed to-13.1 +/- 0.08 and 0.62 +/- 0.03 in diabetic group. It seems that RER cationic channel is involved in metabolic changes which cause by diabetes mellitus and this disease can cause probably a channel gating kinetic and behavior change by inducing metabolic stresses