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Yolk extract-derived vitellogenin 2 ameliorates muscle atrophy in mice via the PI3K/AKT/mTOR pathway
Yilei Li1,2, Peng Song1, Juan Wang3
1College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, Henan 450046, China.
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.
Insights
Egg yolk extract
Area of Science:
- Biochemistry
- Muscle Biology
- Nutritional Science
Background:
- Skeletal muscle atrophy is a significant health concern.
- The active components in egg yolk responsible for muscle development are not well understood.
- Investigating natural compounds for therapeutic potential in muscle wasting conditions is crucial.
Purpose of the Study:
- To determine the effect of vitellogenin 2 (VTG2) from egg yolk extract on muscle atrophy.
- To elucidate the molecular mechanisms underlying VTG2's action in skeletal muscle.
- To explore the therapeutic potential of VTG2 in conditions like cancer cachexia.
Main Methods:
- Proteomic analysis (iTRAK) to identify proteins in egg yolk extracts.
- In vitro studies on myoblast proliferation and differentiation.
- In vivo mouse models of dexamethasone- and cancer cachexia-induced muscle atrophy.
- Analysis of signaling pathways including PI3K/AKT/mTOR, autophagy, inflammation, and mitochondrial function.
Main Results:
- Vitellogenin 2 (VTG2) was identified as a highly expressed protein in egg yolk extracts.
- VTG2 promoted myoblast proliferation and differentiation in vitro.
- VTG2 ameliorated muscle atrophy in vivo, improving P-AKT levels and mitigating autophagy, inflammation, and mitochondrial dysfunction.
- The PI3K/AKT/mTOR pathway was identified as a key mediator of VTG2's effects.
Conclusions:
- Fertilized egg yolk extract (FEYE) improves skeletal muscle atrophy via VTG2.
- VTG2 acts through the PI3K/AKT/mTOR signaling pathway.
- VTG2 demonstrates significant potential for preventing and treating muscle atrophy-related diseases.
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