Maslinic Acid Attenuates Denervation-Induced Loss of Skeletal Muscle Mass and Strength.

Yuki Yamauchi,Farhana Ferdousi,Hiroko Isoda,Satoshi Fukumitsu

doi:10.3390/nu13092950

Abstract

Maslinic acid (MA) is a pentacyclic triterpene abundant in olive peels. MA reportedly increases skeletal muscle mass and strength in older adults; however, the underlying mechanism is unknown. This study aimed to investigate the effects of MA on denervated muscle atrophy and strength and to explore the underlying molecular mechanism. Mice were fed either a control diet or a 0.27% MA diet. One week after intervention, the sciatic nerves of both legs were cut to induce muscle atrophy. Mice were examined 14 days after denervation. MA prevented the denervation-induced reduction in gastrocnemius muscle mass and skeletal muscle strength. Microarray gene expression profiling in gastrocnemius muscle demonstrated several potential mechanisms for muscle maintenance. Gene set enrichment analysis (GSEA) revealed different enriched biological processes, such as myogenesis, PI3/AKT/mTOR signaling, TNFα signaling via NF-κB, and TGF-β signaling in MA-treated mice. In addition, qPCR data showed that MA induced Igf1 expression and suppressed the expressions of Atrogin-1, Murf1 and Tgfb. Altogether, our results suggest the potential of MA as a new therapeutic and preventive dietary ingredient for muscular atrophy and strength.

Highlights

Skeletal muscle makes up about 40% of body weight and is crucial for maintaining an ideal quality of life and achieving superior athletic performance [1]
There were no significant differences in the average daily intake of food (Figure 1A) and body weight (BW) (Figure 1B) between the two groups of mice
We found that Maslinic acid (MA) downregulated the expressions of F-box protein 32 (Fbxo32 / Atrogin-1), forkhead box O1 (Foxo1), Kruppel-like factor 1 (Klf1), growth arrest and DNA-damage-inducible 45 (Gadd45), and phosphatase and tensin homolog (Pten), whereas it upregulated the expressions of Igf1, superoxide dismutase 2, mitochondrial (Sod2), and catalase (Cat), all of which are implicated in FoxO signaling

Summary

Introduction

Skeletal muscle makes up about 40% of body weight and is crucial for maintaining an ideal quality of life and achieving superior athletic performance [1]. Sarcopenia is a condition in which muscle mass and strength decrease due to the gradual decline in skeletal muscle content with aging, which reduces overall muscle quality [3]. It is a major health problem among the elderly and increases the risk of disability, falls, fall-related injuries, hospitalization, dependence, and mortality [4]. The constituent proteins of skeletal myocytes are constantly being degraded and synthesized. Muscle atrophy is the loss of muscle mass due to the imbalance between protein degradation and synthesis [5]. Insulin-like growth factor 1 (IGF-1) induces protein synthesis in skeletal muscle and induces muscle hypertrophy through modulating

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