Work

6′-sialyllactose prevents dexamethasone-induced muscle atrophy by controlling the muscle protein degradation pathway

Year: 2024

Type: article

Abstract: Sarcopenia is associated with various geriatric diseases, such as gait disorders, falls, malnutrition, and osteoporosis. Accordingly, interest in the prevention and treatment of sarcopenia has grown over the years. The human milk oligosaccharide (HMO) 6′-sialyllactose (6′-SL) is known to improve exercise performance, reduce muscle fatigue, and improve GNE myopathy; however, its effect on sarcopenia has not yet been reported. In this study, we aimed to investigate the efficacy of 6′-SL in dexamethasone-induced muscle atrophy, which is a widely used model for the study of sarcopenia. The effects of 6′-SL on differentiated C2C12 skeletal muscle cells and on mice were examined by treatment with 6′-SL in the presence or absence of dexamethasone. 6′-SL was found to inhibit the dexamethasone-induced decrease of MHC expression, as well as to prevent reduction in the number, length, and width of myotubes. Furthermore, the dexamethasone-induced upregulation of myostatin, muscle RING-finger protein-1 (MuRF1), and atrogin-1 were also inhibited by 6′-SL treatment. In mice, intraperitoneal administration of dexamethasone caused decreases in muscle fiber diameter, muscle weight, and exercise performance, most of which were significantly inhibited by oral treatment with 6′-SL. Therefore, utilization of 6′-SL could contribute to the prevention and treatment of muscle atrophy and sarcopenia. • The efficacy of 6′-sialyllactose (6′-SL) in dexamethasone-induced muscle atrophy was investigated. • 6′-SL prevented the decreased MHC expression and the reduced myotubes in dexamethasone-induced muscle atrophy. • 6′-SL prevented the up-regulated expression of myostatin, MuRF1, and atrogin-1 in dexamethasone-induced muscle atrophy. • In mice, 6′-SL prevented the reduced muscle fiber size and exercise performance in dexamethasone-induced muscle atrophy. • It might aid the prevention and treatment of muscle atrophy and sarcopenia.

Source: Biochemical and Biophysical Research Communications

DOI: 10.1016/j.bbrc.2024.150892

Authors: Hiroe Go, Nam Ji Sung, Jaeil Choi, Lila Kim, Eun Jung Park

Institution: Pusan National University Yangsan Hospital

Language: English

Topic: Muscle Physiology and Disorders

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $2,880