Melatonin and Exercise Counteract Sarcopenic Obesity through Preservation of Satellite Cell Function.
Sakulrat MankhongSujin KimSohee MoonJae-Seon LeeEun-Jeong ChoHyo-Bum KwakDong-Ho ParkJi-Kan RyuJu-Hee KangPublished in: International journal of molecular sciences (2023)
Sarcopenic obesity (SO) is characterized by atrophic skeletal muscle impairment (sarcopenia) and obesity, which is associated with adverse outcomes of morbidity and mortality in elderly people. We investigated the effects of melatonin and exercise training on SO in 32-week-old senescence-accelerated mouse-prone-8 (SAMP8) mice fed a normal diet or a high-fat diet for 16 weeks. Melatonin, exercise, or melatonin and exercise for 8 weeks displayed reductions in the SO-induced impairment of skeletal muscle function and atrophy. Specifically, a decrease in mitochondrial calcium retention capacity in skeletal muscles observed in the HFD-con group was attenuated in melatonin and/or exercise intervention groups. More importantly, HFD-con mice displayed a lower number of Pax7+ satellite cells (SCs) and higher expression of p16 ink than P8ND mice, which were attenuated by melatonin and/or exercise interventions. The cellular senescence in SC-derived primary myoblasts from HFD-con mice was significantly attenuated in myoblasts from the melatonin and/or exercise groups, which was reproduced in a senescence model of H 2 O 2 -treated C2C12 myoblasts. Our results suggest that melatonin and exercise training attenuate SO-induced skeletal muscle dysfunction, at least in part, through preserving the SC pool by inhibiting cellular senescence and attenuating mitochondrial dysfunction.
Keyphrases
- insulin resistance
- skeletal muscle
- high fat diet
- high fat diet induced
- high intensity
- physical activity
- adipose tissue
- type diabetes
- weight loss
- metabolic syndrome
- resistance training
- dna damage
- randomized controlled trial
- stress induced
- endothelial cells
- oxidative stress
- induced apoptosis
- diabetic rats
- poor prognosis
- body mass index
- drug induced
- cell proliferation
- mass spectrometry