ABSTRACT
The weight of skeletal muscle accounts for approximately 40% of the whole weight in a healthy individual, and the normal metabolism and motor function of the muscle are indispensable for healthy life. In addition, the skeletal muscle of the maxillofacial region plays an important role not only in eating and swallowing, but also in communication, such as facial expressions and conversations. In recent years, skeletal muscle atrophy has received worldwide attention as a serious health problem. However, the mechanism of skeletal muscle atrophy that has been clarified at present is insufficient, and a therapeutic method against skeletal muscle atrophy has not been established. This review provides views on the importance of skeletal muscle in the maxillofacial region and explains the differences between skeletal muscles in the maxillofacial region and other regions. We summarize the findings to change in gene expression in muscle remodeling and emphasize the advantages and disadvantages of denervation-induced skeletal muscle atrophy model. Finally, we discuss the newly discovered beneficial effects of natural compounds on skeletal muscle atrophy.
Subject(s)
Biological Products/pharmacology , Denervation/adverse effects , Muscle, Skeletal/drug effects , Muscular Atrophy/prevention & control , Animals , Humans , Muscle, Skeletal/pathology , Muscular Atrophy/etiology , Muscular Atrophy/pathologyABSTRACT
Honeybees produce royal jelly (RJ) from their cephalic glands. Royal jelly is a source of nutrition for the queen honey bee throughout its lifespan and is also involved in fertility and longevity. Royal jelly has long been considered beneficial to human health. We recently observed that RJ delayed impairment of motor function during aging, affecting muscle fiber size. However, how RJ affects skeletal muscle metabolism and the functional component of RJ is as of yet unidentified. We demonstrate that feeding mice with RJ daily prevents a decrease in myofiber size following denervation without affecting total muscle weight. RJ did not affect atrophy-related genes but stimulated the expression of myogenesis-related genes, including IGF-1 and IGF receptor. Trans-10-hydroxy-2-decenoic acid (10H2DA) and 10-hydroxydecanoic acid (10HDAA), two major fatty acids contained in RJ. After ingestion, 10H2DA and 10HDAA are metabolized into 2-decenedioic acid (2DA) and sebacic acid (SA) respectively. We found that 10H2DA, 10HDAA, 2DA, and SA all regulated myogenesis of C2C12 cells, murine myoblast cells. These novel findings may be useful for potential preventative and therapeutic applications for muscle atrophy disease included in Sarcopenia, an age-related decline in skeletal muscle mass and strength.
Subject(s)
Decanoic Acids/pharmacology , Denervation/adverse effects , Fatty Acids, Monounsaturated/pharmacology , Fatty Acids/administration & dosage , Muscle Development/drug effects , Muscle, Skeletal/physiology , Muscular Atrophy/prevention & control , Muscular Atrophy/therapy , Myoblasts/physiology , Peptide Hydrolases/administration & dosage , Administration, Oral , Animals , Cells, Cultured , Decanoic Acids/administration & dosage , Decanoic Acids/isolation & purification , Fatty Acids/chemistry , Fatty Acids, Monounsaturated/administration & dosage , Fatty Acids, Monounsaturated/isolation & purification , Insulin-Like Growth Factor I/metabolism , Mice, Inbred C57BL , Muscle Development/genetics , Muscle, Skeletal/physiopathology , Muscular Atrophy/etiology , Receptor, IGF Type 1/metabolism , Sarcopenia/prevention & control , Sarcopenia/therapyABSTRACT
BACKGROUND/AIM: Geranylgeraniol (GGOH), a C20 isoprenoid naturally occurs in several foods. We previously reported that GGOH treatment reduced the expression levels of Atrogin-1 which is involved in skeletal muscle degradation and stimulates the myogenic differentiation of C2C12 myoblasts. However, the effect of GGOH supplementation on skeletal muscle metabolism in vivo is unknown. MATERIALS AND METHODS: Skeletal muscle atrophy was induced by denervation. The expression levels of Atrogin-1 were assessed by western blotting or real time PCR. RESULTS: Intraoral administration of GGOH reduced the decrease in the cross-sectional area of muscle fibers and also suppressed the expression levels of Atrogin-1 in denervation induced muscle atrophy. Also, GGOH treatment suppressed the expression of Atrogin-1 and the decrease in skeletal muscle fiber size by glucocorticoid in vitro. CONCLUSION: Intraoral administration of GGOH rescues denervation-induced muscle atrophy via suppression of Atrogin-1.