Transcutaneous carbon dioxide attenuates impaired oxidative capacity in skeletal muscle in hyperglycemia model
General Physiology and Biophysics
Hyperglycemia impairs oxidative capacity in skeletal muscle. Muscle oxidative capacity is regulated by peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α). Transcutaneous carbon dioxide (CO 2 ) enhances PGC-1α expression in skeletal muscle. Therefore, the aim of this study was to clarify the effects of CO 2 therapy on muscle oxidative capacity impaired by streptozotocin (STZ)induced hyperglycemia. Eight-week-old male Wistar rats were randomly divided into 4 groups: control, CO
... groups: control, CO 2 treatment, STZ-induced hyperglycemia, and STZ-induced hyperglycemia treated with CO 2 . STZinduced hyperglycemia resulted in a decrease of muscle oxidative capacity and decreased PGC-1α and cytochrome c oxidase subunit 4 (COX-4) expression levels; while, application of transcutaneous CO 2 attenuated this effect, and enhanced the expression levels of endothelial nitric oxide synthesis (eNOS). These results indicate that transcutaneous CO 2 improves impaired muscle oxidative capacity via enhancement of eNOS and PGC-1α-related signaling in the skeletal muscle of rats with hyperglycemia.