Mitigation of high-fat diet-induced sarcopenia by fruit extracts via autophagic flux and mitochondrial quality control.

UNLABELLED

Sarcopenic obesity, encompassing both muscle wasting and obesity, is relevant across individuals. (TS) has been shown to regulate glucose and lipid metabolisms. However, the efficacy and mechanisms of TS fruit (TSF) in sarcopenic obesity are unclear. This study investigated impacts of TSF extract on skeletal muscle atrophy in C57BL/6 mice fed a high-fat diet (HFD). After 25 weeks of TSF pre-treatment and supplementation, it reversed loss of skeletal muscle mass and grip strength in HFD-fed mice, independent of body weight changes. TSF treatment notably increased the phosphorylation of Akt, mTOR, and P70S6K, while suppressing nuclear localization of NFκB, FoxO1a, and transcription of atrogin-1, MuRF-1, and myostatin expression in HFD-fed muscle. Additionally, TSF influenced autophagic flux and mitochondria quality control, emphasizing its role in balancing protein synthesis and degradation. In conclusion, TSF alleviates HFD-induced sarcopenia via protein turnover, autophagic flux and mitochondria quality control, highlighting its potential therapeutic value for sarcopenic obesity.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s10068-024-01610-3.