Brain mitochondrial 93 pS cationic channel activities impaired in diabetic rats

Evidence indicates an impairment of mitochondrial functions and alterations in potassium channel activities in diabetes mellitus. This study was carried out to consider whether the biophysical properties of the mitochondrial 93 pS cationic channel are altered in diabetes.

Diabetes mellitus was induced in male Wistar rats (200-250 g) by single intraperitoneal injection of 45 mg/kg streptozotocin dissolved in 0.1 M citrate buffer (pH 4.5). The brain mitochondrial inner membranes were extracted and vesicles were incorporated into lipid bilayer membranes, and single potassium channel properties were evaluated. Purity of the cell fraction was also tested by Western blotting. Data were analyzed by Makov noise free single channel analysis.

Based on our previous data, mitochondrial inner membrane has a potassium channel with a main conductance of 93 pS, which was 4-AP-sensitive and voltage-insensitive at -50 to +50 mV. Our data showed that channel conductance decreased to 48 pS and inwardly rectifying current voltage curve was altered to an ohmic behavior in vesicles of diabetic rats but there was no effect on channel open probability. Western blotting and antibodies directed against various cellular proteins revealed that the extracted material contains only mitochondria.

Our data showed that the biophysical properties (conductance) of potassium channel were significantly altered in diabetes. Based on these findings, we propose that the brain mitochondrial potassium channels are involved in diabetes, and it can be considered as a target for therapeutic plans.