Nagato Kuriyama1, Etsuko Ozaki2, Teruhide Koyama2, Daisuke Matsui2, Isao Watanabe2, Satomi Tomida2,3, Reo Nagamitsu2, Kanae Hashiguchi2, Masaaki Inaba4, Shinsuke Yamada4, Motoyuki Horii5, Shigeto Mizuno6, Yutaro Yoneda3, Masao Kurokawa7, Daiki Kobayashi8, Shinpei Fukuda9, Koichi Iwasa10, Yoshiyuki Watanabe2, Ritei Uehara2. 1. Department of Epidemiology for Community Health and Medicine, Kyoto Prefectural University of Medicine, 465 Kajiicho, Kawaramachi-hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan. nkuriyam@koto.kpu-m.ac.jp. 2. Department of Epidemiology for Community Health and Medicine, Kyoto Prefectural University of Medicine, 465 Kajiicho, Kawaramachi-hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan. 3. Department of Endocrine and Breast Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan. 4. Department of Metabolism, Endocrinology, and Molecular Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan. 5. Department of Orthopaedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan. 6. Department of Endoscopy, Kindai University Nara Hospital, Ikoma City, Nara Prefecture, Japan. 7. Department of Orthopaedics, Saiseikai Suita Hospital, Osaka, Japan. 8. Division of General Internal Medicine, Department of Medicine, St. Luke's International Hospital, Tokyo, Japan. 9. Department of Health Promoting and Geriatric Acupuncture and Moxibustion, Meiji University of Integrative Medicine, Kyoto, Japan. 10. Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Abstract
INTRODUCTION: Bone mass was recently reported to be related to skeletal muscle mass in humans, and a decrease in cortical bone is a risk factor for osteoporosis. Because circulating myostatin is a factor that primarily controls muscle metabolism, this study examined the role of myostatin in bone mass-skeletal muscle mass interactions. METHODS: The subjects were 375 middle-aged community residents with no history of osteoporosis or sarcopenia who participated in a health check-up. Cortical bone thickness and cancellous bone density were measured by ultrasonic bone densitometry in a health check-up survey. The subjects were divided into those with low cortical bone thickness (LCT) or low cancellous bone density (LBD) and those with normal values (NCT/NBD). Bone metabolism markers (TRACP-5b, etc.), skeletal muscle mass, serum myostatin levels, and lifestyle were then compared between the groups. RESULTS: The percentage of diabetic participants, TRACP-5b, and myostatin levels were significantly higher, and the frequency of physical activity, skeletal muscle mass, grip strength, and leg strength were significantly lower in the LCT group than in the NCT group. The odds ratio (OR) of high myostatin levels in the LCT group compared with the NCT group was significant (OR 2.17) even after adjusting for related factors. Between the low cancellous bone density (LBD) and normal cancellous bone density (NBD) groups, significant differences were observed in the same items as between the LCT and NCT groups, but no significant differences were observed in skeletal muscle mass and blood myostatin levels. The myostatin level was significantly negatively correlated with cortical bone thickness and skeletal muscle mass. CONCLUSIONS: A decrease in cortical bone thickness was associated with a decrease in skeletal muscle mass accompanied by an increase in the blood myostatin level. Blood myostatin may regulate the bone-skeletal muscle relationship and serve as a surrogate marker of bone metabolism, potentially linking muscle mass to bone structure.
INTRODUCTION: Bone mass was recently reported to be related to skeletal muscle mass in humans, and a decrease in cortical bone is a risk factor for osteoporosis. Because circulating myostatin is a factor that primarily controls muscle metabolism, this study examined the role of myostatin in bone mass-skeletal muscle mass interactions. METHODS: The subjects were 375 middle-aged community residents with no history of osteoporosis or sarcopenia who participated in a health check-up. Cortical bone thickness and cancellous bone density were measured by ultrasonic bone densitometry in a health check-up survey. The subjects were divided into those with low cortical bone thickness (LCT) or low cancellous bone density (LBD) and those with normal values (NCT/NBD). Bone metabolism markers (TRACP-5b, etc.), skeletal muscle mass, serum myostatin levels, and lifestyle were then compared between the groups. RESULTS: The percentage of diabeticparticipants, TRACP-5b, and myostatin levels were significantly higher, and the frequency of physical activity, skeletal muscle mass, grip strength, and leg strength were significantly lower in the LCT group than in the NCT group. The odds ratio (OR) of high myostatin levels in the LCT group compared with the NCT group was significant (OR 2.17) even after adjusting for related factors. Between the low cancellous bone density (LBD) and normal cancellous bone density (NBD) groups, significant differences were observed in the same items as between the LCT and NCT groups, but no significant differences were observed in skeletal muscle mass and blood myostatin levels. The myostatin level was significantly negatively correlated with cortical bone thickness and skeletal muscle mass. CONCLUSIONS: A decrease in cortical bone thickness was associated with a decrease in skeletal muscle mass accompanied by an increase in the blood myostatin level. Blood myostatin may regulate the bone-skeletal muscle relationship and serve as a surrogate marker of bone metabolism, potentially linking muscle mass to bone structure.
Entities:
Keywords:
Bone–muscle relationship; Cortical bone; Myostatin; Skeletal muscle mass
Authors: Ann V Schwartz; Eric Vittinghoff; Douglas C Bauer; Teresa A Hillier; Elsa S Strotmeyer; Kristine E Ensrud; Meghan G Donaldson; Jane A Cauley; Tamara B Harris; Annemarie Koster; Catherine R Womack; Lisa Palermo; Dennis M Black Journal: JAMA Date: 2011-06-01 Impact factor: 56.272
Authors: Ling Oei; M Carola Zillikens; Abbas Dehghan; Gabriëlle H S Buitendijk; Martha C Castaño-Betancourt; Karol Estrada; Lisette Stolk; Edwin H G Oei; Joyce B J van Meurs; Joseph A M J L Janssen; Albert Hofman; Johannes P T M van Leeuwen; Jacqueline C M Witteman; Huibert A P Pols; André G Uitterlinden; Caroline C W Klaver; Oscar H Franco; Fernando Rivadeneira Journal: Diabetes Care Date: 2013-01-11 Impact factor: 19.112