Yolk extract-derived vitellogenin 2 ameliorates muscle atrophy in mice via the PI3K/AKT/mTOR pathway

Abstract

Eggs play an important role in skeletal muscle development, but their active components are unknown. The aim of this study was to investigate the effect of yolk extract-derived vitellogenin 2 on dexamethasone (DEX)- and cancer cachexia (CC)-induced skeletal muscle atrophy. We used iTRAQ to detect the changes in protein expression between fertilized egg yolk extract (FEYE) and unfertilized egg yolk extract (UEYE). Results showed that 15 proteins were up-regulated and 1 protein was down-regulated, and the expression of VTG2 (vitellogenin 2) was the highest in both FEYE and UEYE. Further research demonstrated that VTG2 can promote the proliferation and differentiation of myoblasts in vitro. We later proved that VTG2 not only improved the muscle atrophy in 7-week-old male C57BL/6 mice but also inhibited the decrease in P-AKT levels induced by the muscle atrophy model. At the same time, it was proved that VTG2 can improve autophagy, inflammation and mitochondrial dysfunction caused in a myotube atrophy model. Subsequent research proved that PI3K/AKT/mTOR was considered an important pathway for VTG2 to improve muscle atrophy. Therefore, the above results proved that FEYE can improve muscle atrophy through the PI3K/AKT/mTOR pathway mediated by VTG2. This study clarified the role of VTG2 in skeletal muscle atrophy and proved that VTG2 has potential application value in the prevention of diseases related to skeletal muscle atrophy.