Effect of lactate administration on mouse skeletal muscle under calorie restriction.
Autophagy
Calorie restriction
Keywards
Lactate
Skeletal muscle
mTOR signaling
Journal
Current research in physiology
ISSN: 2665-9441
Titre abrégé: Curr Res Physiol
Pays: Netherlands
ID NLM: 101769251
Informations de publication
Date de publication:
2021
2021
Historique:
received:
26
05
2021
revised:
25
08
2021
accepted:
03
09
2021
entrez:
8
11
2021
pubmed:
9
11
2021
medline:
9
11
2021
Statut:
epublish
Résumé
Calorie restriction (CR) involves a reductions of calorie intake without altering the nutritional balance, and has many beneficial effects, such as improving oxidative metabolism and extending lifespan. However, CR decreases in skeletal muscle mass and fat mass in correlation with the reduction in food intake. Lactate is known to have potential as a signaling molecule rather than a metabolite during exercise. In this study, we examined the effects of the combination of caloric restriction and lactate administration on skeletal muscle adaptation in order to elucidate a novel role of lactate. We first demonstrated that daily lactate administration (equivalent to 1 g/kg of body weight) for 2 weeks suppressed CR-induced muscle atrophy by activating mammalian/mechanistic target of rapamycin (mTOR) signaling, a muscle protein synthesis pathway, and inhibited autophagy-induced muscle degradation. Next, we found that lactate administration under calorie restriction enhanced mitochondrial enzyme activity (citrate synthase and succinate dehydrogenase) and the expression of oxidative phosphorylation (OXPHOS) protein expression. Our results suggest that lactate administration under caloric restriction not only suppresses muscle atrophy but also improves mitochondrial function.
Identifiants
pubmed: 34746839
doi: 10.1016/j.crphys.2021.09.001
pii: S2665-9441(21)00022-5
pmc: PMC8562144
doi:
Types de publication
Journal Article
Langues
eng
Pagination
202-208Informations de copyright
© 2021 The Author(s).
Déclaration de conflit d'intérêts
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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