Aki Miyawaki1,2, Thira Rojasawasthien1, Suzuro Hitomi3, Yoshinori Aoki4, Mariko Urata1, Asako Inoue1, Takuma Matsubara1, Kazumasa Morikawa5, Manabu Habu2, Kazuhiro Tominaga2, Shoichiro Kokabu6. 1. Division of Molecular Signaling and Biochemistry, Department of Health Improvement, Kyushu Dental University, Kitakyushu, Japan. 2. Division of Oral and Maxillofacial Surgery, Department of Science and Physical Functions, Kyushu Dental University, Kitakyushu, Japan. 3. Department of Physiology, Nihon University School of Dentistry, Tokyo, Japan. 4. Foods and Nutrition Science Div. Mitsubishi-Chemical Foods Corporation, Tokyo, Japan. 5. Division of Pediatric and Special Care Dentistry, Department of Developmental Oral Health Science, School of Dentistry, Iwate Medical University, Morioka, Japan. 6. Division of Molecular Signaling and Biochemistry, Department of Health Improvement, Kyushu Dental University, Kitakyushu, Japan r14kokabu@fa.kyu-dent.ac.jp.
Abstract
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. Copyright
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. Copyright