Limosilactobacillus reuteri ATG-F4 Improves the Muscle Strength and Muscle Mass of Mice with Immobilization-Induced Muscular Atrophy
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Probiotics offer a promising avenue for combating muscle atrophy, which is a debilitating condition associated with muscle disuse, aging, and disease. This study investigated the anti-atrophic potential of Limosilactobacillus reuteri ATG-F4, a human gut-derived bacterium, in a mouse model of stapleinduced immobilization. ATG-F4 administration significantly preserved muscle mass and improved grip strength and endurance. Mechanistically, ATG-F4 activated mTOR signaling and promoted protein synthesis. Additionally, ATG-F4 downregulated MuRF1, a key atrophy factor. Furthermore, ATG-F4 administration significantly altered the composition of the gut microbiota, favoring the presence of the Muribaculaceae family and decreasing the abundance of Lachnospiraceae and Lactobacillaceae. Administration of ATG-F4 increased serum levels of the short-chain fatty acids (SCFAs) butyrate and acetate. SCFAs, which are produced by bacterial fermentation in the gut, possess anti-inflammatory and beneficial muscle properties and exert several effects on host metabolism and the immune system. Therefore, we suggest that the potential mechanism underlying the anti-atrophic effects of ATG-F4 on muscles involves the enhancement of muscle protein synthesis, suppression of protein degradation, and modulation of the gut-muscle axis. These findings highlight the potential of ATG-F4 as a prophylactic or therapeutic agent for the treatment of muscle atrophy.
Abstract
Probiotics offer a promising avenue for combating muscle atrophy, which is a debilitating condition associated with muscle disuse, aging, and disease. This study investigated the anti-atrophic potential of Limosilactobacillus reuteri ATG-F4, a human gut-derived bacterium, in a mouse model of stapleinduced immobilization. ATG-F4 administration significantly preserved muscle mass and improved grip strength and endurance. Mechanistically, ATG-F4 activated mTOR signaling and promoted protein synthesis. Additionally, ATG-F4 downregulated MuRF1, a key atrophy factor. Furthermore, ATG-F4 administration significantly altered the composition of the gut microbiota, favoring the presence of the Muribaculaceae family and decreasing the abundance of Lachnospiraceae and Lactobacillaceae. Administration of ATG-F4 increased serum levels of the short-chain fatty acids (SCFAs) butyrate and acetate. SCFAs, which are produced by bacterial fermentation in the gut, possess anti-inflammatory and beneficial muscle properties and exert several effects on host metabolism and the immune system. Therefore, we suggest that the potential mechanism underlying the anti-atrophic effects of ATG-F4 on muscles involves the enhancement of muscle protein synthesis, suppression of protein degradation, and modulation of the gut-muscle axis. These findings highlight the potential of ATG-F4 as a prophylactic or therapeutic agent for the treatment of muscle atrophy.