Naringenin promotes the expression of oxidized myofibers via the PKA signaling pathway in C57BL/6J mice and C2C12 cells

Abstract

Naringenin, a citrus-derived flavonoid, has been reported to positively exert skeletal muscle function. The study designed to explore the potential role and mechanisms of naringenin on regulating the expression of oxidized myofibrils in mice and C2C12 myotubes. In this study, we found that naringenin supplementation significantly improved exercise endurance and oxygen consumption of mice, and also increased aerobic enzyme activity and oxidative myofibers expression in skeletal muscle and C2C12 cells. Meanwhile, naringenin activated the expression of p-PKA/PKA, p-LKB1/LKB1, p-AMPK/AMPK and PGC-1α in skeletal muscle. Furthermore, in vitro studies shown that inhibition of PKA, LKB1 and AMPK could attenuate naringenin-regulated increase in slow muscle fiber proteins. This study suggests that naringenin supplementation can enhance slow myofiber expression by activating the PKA signaling pathway in C57BL/6J mice and C2C12 myotubes. These findings provide a new application of naringenin as a natural candidate to regulate oxidized fiber types and endurance of skeletal muscle.