Glibenclamide Elicits Endoplasmic Reticulum Stress and Myokine Expression in the L6 Skeletal Muscle Cells

Although glibenclamide is an oral hypoglycemic agent used in type 2 diabetes, skeletal muscle wasting has been reported as a side effect. To understand how to reduce this side effect, we determined whether glibenclamide induces endoplasmic reticulum (ER) stress in skeletal muscle cells and which myokine expression changes at this time. The ER chaperone genes do not show a significant change by glibenclamide, but the ER stress sensor genes are upexpressed approximately twice, and those downstream [ATF6 (activating transcription factor 6) fragmentation, eIF2α (eukaryotic initiation factor-2α) phosphorylation, and XBP1 (Xbox DNA-binding protein) mRNA splicing] are activated. Additionally, the myokine gene expression was up- or downregulated by glibenclamide. These results will serve as useful data for overcoming the side effects of sarcopenia caused by glibenclamide.