Authors: Khodaee, Naser
Ghasemi, Maedeh
Saghiri, Reza
Eliassi, Afsaneh
Title: Endoplasmic reticulum membrane potassium channel dysfunction in high fat diet induced stress in rat hepatocytes
Language (ISO): en
Abstract: In a previous study we reported the presence of a large conductance K+ channel in the membrane of endoplasmic reticulum (ER) from rat hepatocytes. The channel open probability (Po) appeared voltage dependent and reached to a minimum 0.2 at +50 mV. Channel activity in this case was found to be totally inhibited at ATP concentration 2.5 mM, glibenclamide 100 μM and tolbutamide 400 μM. Existing evidence indicates an impairment of endoplasmic reticulum functions in ER stress condition. Because ER potassium channels have been involved in several ER functions including cytoprotection, apoptosis and calcium homeostasis, a study was carried out to consider whether the ER potassium channel function is altered in a high fat diet model of ER stress. Male Wistar rats were made ER stress for 2 weeks with a high fat diet. Ion channel incorporation of ER stress model into the bilayer lipid membrane allowed the characterization of K+ channel. Our results indicate that the channel Po was significantly increased at voltages above +30 mV. Interestingly, addition of ATP 7.5 mM, glibenclamide 400 μM and tolbutamide 2400 μM totally inhibited the channel activities, 3-fold, 4-fold and 6-fold higher than that in the control groups, respectively. Our results thus demonstrate a modification in the ER K+ channel gating properties and decreased sensitivity to drugs in membrane preparations coming from ER high fat model of ER stress, an effect potentially linked to a change in ER K+ channel subunits in ER stress condition. Our results may provide new insights into the cellular mechanisms underlying ER dysfunctions in ER stress.
Subject Headings: endoplasmic reticulum
potassium channel
ER stress
bilayer lipid membrane
hepatocytes
URI: http://hdl.handle.net/2003/33733
http://dx.doi.org/10.17877/DE290R-7039
Issue Date: 2014-09-09
Appears in Collections:Original Articles

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