Evaluation of myostatin as a possible regulator and marker of skeletal muscle–cortical bone interaction in adults
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...
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| Veröffentlicht in: | Journal of bone and mineral metabolism 2021-05, Vol.39 (3), p.404-415 |
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| creator | Kuriyama, Nagato Ozaki, Etsuko Koyama, Teruhide Matsui, Daisuke Watanabe, Isao Tomida, Satomi Nagamitsu, Reo Hashiguchi, Kanae Inaba, Masaaki Yamada, Shinsuke Horii, Motoyuki Mizuno, Shigeto Yoneda, Yutaro Kurokawa, Masao Kobayashi, Daiki Fukuda, Shinpei Iwasa, Koichi Watanabe, Yoshiyuki Uehara, Ritei |
| description | 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. |
| doi_str_mv | 10.1007/s00774-020-01160-8 |
| format | Article |
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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.</description><identifier>ISSN: 0914-8779</identifier><identifier>EISSN: 1435-5604</identifier><identifier>DOI: 10.1007/s00774-020-01160-8</identifier><identifier>PMID: 33044569</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Acid phosphatase (tartrate-resistant) ; Adult ; Biomarkers - metabolism ; Blood levels ; Bone density ; Bone Density - physiology ; Bone mass ; Bone turnover ; Cancellous bone ; Cortical bone ; Cortical Bone - metabolism ; Densitometry ; Diabetes mellitus ; Female ; Humans ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolism ; Middle Aged ; Multivariate Analysis ; Muscle, Skeletal - metabolism ; Musculoskeletal system ; Myostatin ; Myostatin - metabolism ; Organ Size ; Original Article ; Orthopedics ; Osteoporosis ; Physical activity ; Regression Analysis ; Risk factors ; Sarcopenia ; Skeletal muscle</subject><ispartof>Journal of bone and mineral metabolism, 2021-05, Vol.39 (3), p.404-415</ispartof><rights>The Japanese Society Bone and Mineral Research and Springer Japan KK, part of Springer Nature 2020</rights><rights>The Japanese Society Bone and Mineral Research and Springer Japan KK, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c465t-3c348bab2dd5ebfc702e5b791157ef2c3473ed0c017f08355236aad5b032bab03</citedby><cites>FETCH-LOGICAL-c465t-3c348bab2dd5ebfc702e5b791157ef2c3473ed0c017f08355236aad5b032bab03</cites><orcidid>0000-0002-6859-535X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00774-020-01160-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00774-020-01160-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33044569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuriyama, Nagato</creatorcontrib><creatorcontrib>Ozaki, Etsuko</creatorcontrib><creatorcontrib>Koyama, Teruhide</creatorcontrib><creatorcontrib>Matsui, Daisuke</creatorcontrib><creatorcontrib>Watanabe, Isao</creatorcontrib><creatorcontrib>Tomida, Satomi</creatorcontrib><creatorcontrib>Nagamitsu, Reo</creatorcontrib><creatorcontrib>Hashiguchi, Kanae</creatorcontrib><creatorcontrib>Inaba, Masaaki</creatorcontrib><creatorcontrib>Yamada, Shinsuke</creatorcontrib><creatorcontrib>Horii, Motoyuki</creatorcontrib><creatorcontrib>Mizuno, Shigeto</creatorcontrib><creatorcontrib>Yoneda, Yutaro</creatorcontrib><creatorcontrib>Kurokawa, Masao</creatorcontrib><creatorcontrib>Kobayashi, Daiki</creatorcontrib><creatorcontrib>Fukuda, Shinpei</creatorcontrib><creatorcontrib>Iwasa, Koichi</creatorcontrib><creatorcontrib>Watanabe, Yoshiyuki</creatorcontrib><creatorcontrib>Uehara, Ritei</creatorcontrib><title>Evaluation of myostatin as a possible regulator and marker of skeletal muscle–cortical bone interaction in adults</title><title>Journal of bone and mineral metabolism</title><addtitle>J Bone Miner Metab</addtitle><addtitle>J Bone Miner Metab</addtitle><description>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.</description><subject>Acid phosphatase (tartrate-resistant)</subject><subject>Adult</subject><subject>Biomarkers - metabolism</subject><subject>Blood levels</subject><subject>Bone density</subject><subject>Bone Density - physiology</subject><subject>Bone mass</subject><subject>Bone turnover</subject><subject>Cancellous bone</subject><subject>Cortical bone</subject><subject>Cortical Bone - metabolism</subject><subject>Densitometry</subject><subject>Diabetes mellitus</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Musculoskeletal system</subject><subject>Myostatin</subject><subject>Myostatin - metabolism</subject><subject>Organ Size</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Osteoporosis</subject><subject>Physical activity</subject><subject>Regression Analysis</subject><subject>Risk factors</subject><subject>Sarcopenia</subject><subject>Skeletal muscle</subject><issn>0914-8779</issn><issn>1435-5604</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc9OFTEUxhuDgQvyAi5MEzduRk__TadLQlBJSNzouul0zpCBzvTSdkjY-Q6-oU9iLxcxccGmTXt-33fa8xHylsFHBqA_5bpo2QCHBhhroelekQ2TQjWqBXlANmCYbDqtzRE5zvkGgGml2SE5EgKkVK3ZkHxx78LqyhQXGkc6P8Rc6mmhLlNHtzHnqQ9IE16vwZWYqFsGOrt0i2nH51sMWFyg85p9wN8_f_mYyuTrTR8XpNNSMDn_aL8zHdZQ8hvyenQh4-nTfkJ-fL74fv61ufr25fL87KrxslWlEV7Irnc9HwaF_eg1cFS9NowpjSOvVS1wAF9_NUInlOKidW5QPQheZSBOyIe97zbFuxVzsfOUPYbgFoxrtlxKY4zURlT0_X_oTVzTUl9nuWKGKda1ulJ8T_lUB5NwtNs01WE8WAZ2F4ndR2JrJPYxEttV0bsn67WfcXiW_M2gAmIP5FparjH96_2C7R8YdJkK</recordid><startdate>20210501</startdate><enddate>20210501</enddate><creator>Kuriyama, Nagato</creator><creator>Ozaki, Etsuko</creator><creator>Koyama, Teruhide</creator><creator>Matsui, Daisuke</creator><creator>Watanabe, Isao</creator><creator>Tomida, Satomi</creator><creator>Nagamitsu, Reo</creator><creator>Hashiguchi, Kanae</creator><creator>Inaba, Masaaki</creator><creator>Yamada, Shinsuke</creator><creator>Horii, Motoyuki</creator><creator>Mizuno, Shigeto</creator><creator>Yoneda, Yutaro</creator><creator>Kurokawa, Masao</creator><creator>Kobayashi, Daiki</creator><creator>Fukuda, Shinpei</creator><creator>Iwasa, Koichi</creator><creator>Watanabe, Yoshiyuki</creator><creator>Uehara, Ritei</creator><general>Springer Singapore</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6859-535X</orcidid></search><sort><creationdate>20210501</creationdate><title>Evaluation of myostatin as a possible regulator and marker of skeletal muscle–cortical bone interaction in adults</title><author>Kuriyama, Nagato ; Ozaki, Etsuko ; Koyama, Teruhide ; Matsui, Daisuke ; Watanabe, Isao ; Tomida, Satomi ; Nagamitsu, Reo ; Hashiguchi, Kanae ; Inaba, Masaaki ; Yamada, Shinsuke ; Horii, Motoyuki ; Mizuno, Shigeto ; Yoneda, Yutaro ; Kurokawa, Masao ; Kobayashi, Daiki ; Fukuda, Shinpei ; Iwasa, Koichi ; Watanabe, Yoshiyuki ; Uehara, Ritei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c465t-3c348bab2dd5ebfc702e5b791157ef2c3473ed0c017f08355236aad5b032bab03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acid phosphatase (tartrate-resistant)</topic><topic>Adult</topic><topic>Biomarkers - metabolism</topic><topic>Blood levels</topic><topic>Bone density</topic><topic>Bone Density - physiology</topic><topic>Bone mass</topic><topic>Bone turnover</topic><topic>Cancellous bone</topic><topic>Cortical bone</topic><topic>Cortical Bone - metabolism</topic><topic>Densitometry</topic><topic>Diabetes mellitus</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Multivariate Analysis</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Musculoskeletal system</topic><topic>Myostatin</topic><topic>Myostatin - metabolism</topic><topic>Organ Size</topic><topic>Original Article</topic><topic>Orthopedics</topic><topic>Osteoporosis</topic><topic>Physical activity</topic><topic>Regression Analysis</topic><topic>Risk factors</topic><topic>Sarcopenia</topic><topic>Skeletal muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuriyama, Nagato</creatorcontrib><creatorcontrib>Ozaki, Etsuko</creatorcontrib><creatorcontrib>Koyama, Teruhide</creatorcontrib><creatorcontrib>Matsui, Daisuke</creatorcontrib><creatorcontrib>Watanabe, Isao</creatorcontrib><creatorcontrib>Tomida, Satomi</creatorcontrib><creatorcontrib>Nagamitsu, Reo</creatorcontrib><creatorcontrib>Hashiguchi, Kanae</creatorcontrib><creatorcontrib>Inaba, Masaaki</creatorcontrib><creatorcontrib>Yamada, Shinsuke</creatorcontrib><creatorcontrib>Horii, Motoyuki</creatorcontrib><creatorcontrib>Mizuno, Shigeto</creatorcontrib><creatorcontrib>Yoneda, Yutaro</creatorcontrib><creatorcontrib>Kurokawa, Masao</creatorcontrib><creatorcontrib>Kobayashi, Daiki</creatorcontrib><creatorcontrib>Fukuda, Shinpei</creatorcontrib><creatorcontrib>Iwasa, Koichi</creatorcontrib><creatorcontrib>Watanabe, Yoshiyuki</creatorcontrib><creatorcontrib>Uehara, Ritei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bone and mineral metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kuriyama, Nagato</au><au>Ozaki, Etsuko</au><au>Koyama, Teruhide</au><au>Matsui, Daisuke</au><au>Watanabe, Isao</au><au>Tomida, Satomi</au><au>Nagamitsu, Reo</au><au>Hashiguchi, Kanae</au><au>Inaba, Masaaki</au><au>Yamada, Shinsuke</au><au>Horii, Motoyuki</au><au>Mizuno, Shigeto</au><au>Yoneda, Yutaro</au><au>Kurokawa, Masao</au><au>Kobayashi, Daiki</au><au>Fukuda, Shinpei</au><au>Iwasa, Koichi</au><au>Watanabe, Yoshiyuki</au><au>Uehara, Ritei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evaluation of myostatin as a possible regulator and marker of skeletal muscle–cortical bone interaction in adults</atitle><jtitle>Journal of bone and mineral metabolism</jtitle><stitle>J Bone Miner Metab</stitle><addtitle>J Bone Miner Metab</addtitle><date>2021-05-01</date><risdate>2021</risdate><volume>39</volume><issue>3</issue><spage>404</spage><epage>415</epage><pages>404-415</pages><issn>0914-8779</issn><eissn>1435-5604</eissn><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.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>33044569</pmid><doi>10.1007/s00774-020-01160-8</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6859-535X</orcidid></addata></record> |
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| ispartof | Journal of bone and mineral metabolism, 2021-05, Vol.39 (3), p.404-415 |
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| subjects | Acid phosphatase (tartrate-resistant) Adult Biomarkers - metabolism Blood levels Bone density Bone Density - physiology Bone mass Bone turnover Cancellous bone Cortical bone Cortical Bone - metabolism Densitometry Diabetes mellitus Female Humans Male Medicine Medicine & Public Health Metabolic Diseases Metabolism Middle Aged Multivariate Analysis Muscle, Skeletal - metabolism Musculoskeletal system Myostatin Myostatin - metabolism Organ Size Original Article Orthopedics Osteoporosis Physical activity Regression Analysis Risk factors Sarcopenia Skeletal muscle |
| title | Evaluation of myostatin as a possible regulator and marker of skeletal muscle–cortical bone interaction in adults |
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