Ben Kirk1,2, Jack Feehan1,2, Giovanni Lombardi3,4, Gustavo Duque5,6. 1. Department of Medicine-Western Health, Melbourne Medical School, University of Melbourne, St Albans, VIC, Australia. 2. Australian Institute for Musculoskeletal Science (AIMSS), University of Melbourne and Western Health, St Albans, VIC, Australia. 3. Laboratory of Experimental Biochemistry & Molecular Biology, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy. 4. Department of Athletics, Strength and Conditioning, Poznań University of Physical Education, Poznań, Poland. 5. Department of Medicine-Western Health, Melbourne Medical School, University of Melbourne, St Albans, VIC, Australia. gustavo.duque@unimelb.edu.au. 6. Australian Institute for Musculoskeletal Science (AIMSS), University of Melbourne and Western Health, St Albans, VIC, Australia. gustavo.duque@unimelb.edu.au.
Abstract
PURPOSE OF REVIEW: Skeletal muscle and bone are connected anatomically and physiologically, and play a crucial role in human locomotion and metabolism. Historically, the coupling between muscle and bone has been viewed in light of mechanotransduction, which dictates that the mechanical forces applied to muscle are transmitted to the skeleton to initiate bone formation. However, these organs also communicate through the endocrine system, orchestrated by a family of cytokines namely myokines (derived from myocytes) and osteokines (derived from bone cells). A third player in this biochemical crosstalk is adipose tissue and the secretion of adipokines (derived from adipocytes). In this review, we discuss the bidirectional effects of myokines and osteokines on muscle and bone metabolism, and the impact of adipokines on both of these secretory organs. RECENT FINDINGS: Several myokines, notably, IL6, irisin, IGF-1, BDNF, myostatin, and FGF2 exert anabolic/catabolic effects on bone, while the osteokines osteocalcin and sclerostin have shown to induce muscle anabolism and catabolism, respectively. Adipokines, such as leptin, resistin, adiponectin, and TNFα (released from adipose tissue), can also modulate muscle and bone metabolism. Contrarily, exercise-mediated release of lipolytic myokines (IL6, irisin, and LIF) stimulates thermogenesis by promoting the browning of adipocytes. Myokines, osteokines, and adipokines exert autocrine/paracrine effects locally as well as through the endocrine system, to regulate muscle, bone, and fat metabolism. Reductions in physical activity and increases in energy intake, both linked with aging, leads to adipocyte hypertrophy and the recruitment of immunological cells (macrophages). In turn, this releases pro-inflammatory adipokines which induces chronic low-grade inflammation (LGI), a key player in the pathology of several diseases. However, exercise-induced stimulation of bioactive cytokines, through muscle-bone-fat crosstalk, increases muscle anabolism, bone formation, mitochondrial biogenesis, glucose utilization, and fatty acid oxidation, and attenuates chronic LGI.
PURPOSE OF REVIEW: Skeletal muscle and bone are connected anatomically and physiologically, and play a crucial role in human locomotion and metabolism. Historically, the coupling between muscle and bone has been viewed in light of mechanotransduction, which dictates that the mechanical forces applied to muscle are transmitted to the skeleton to initiate bone formation. However, these organs also communicate through the endocrine system, orchestrated by a family of cytokines namely myokines (derived from myocytes) and osteokines (derived from bone cells). A third player in this biochemical crosstalk is adipose tissue and the secretion of adipokines (derived from adipocytes). In this review, we discuss the bidirectional effects of myokines and osteokines on muscle and bone metabolism, and the impact of adipokines on both of these secretory organs. RECENT FINDINGS: Several myokines, notably, IL6, irisin, IGF-1, BDNF, myostatin, and FGF2 exert anabolic/catabolic effects on bone, while the osteokines osteocalcin and sclerostin have shown to induce muscle anabolism and catabolism, respectively. Adipokines, such as leptin, resistin, adiponectin, and TNFα (released from adipose tissue), can also modulate muscle and bone metabolism. Contrarily, exercise-mediated release of lipolytic myokines (IL6, irisin, and LIF) stimulates thermogenesis by promoting the browning of adipocytes. Myokines, osteokines, and adipokines exert autocrine/paracrine effects locally as well as through the endocrine system, to regulate muscle, bone, and fat metabolism. Reductions in physical activity and increases in energy intake, both linked with aging, leads to adipocyte hypertrophy and the recruitment of immunological cells (macrophages). In turn, this releases pro-inflammatory adipokines which induces chronic low-grade inflammation (LGI), a key player in the pathology of several diseases. However, exercise-induced stimulation of bioactive cytokines, through muscle-bone-fat crosstalk, increases muscle anabolism, bone formation, mitochondrial biogenesis, glucose utilization, and fatty acid oxidation, and attenuates chronic LGI.
Authors: Arnold Z Olali; Qiuhu Shi; Donald R Hoover; Mariana Bucovsky; Elizabeth Shane; Michael T Yin; Ryan D Ross Journal: Bone Date: 2021-09-20 Impact factor: 4.626
Authors: Henrik Pettersson; Helene Alexanderson; Janet L Poole; Janos Varga; Malin Regardt; Anne-Marie Russell; Yasser Salam; Kelly Jensen; Jennifer Mansour; Tracy Frech; Carol Feghali-Bostwick; Cecília Varjú; Nancy Baldwin; Matty Heenan; Kim Fligelstone; Monica Holmner; Matthew R Lammi; Mary Beth Scholand; Lee Shapiro; Elizabeth R Volkmann; Lesley Ann Saketkoo Journal: Best Pract Res Clin Rheumatol Date: 2021-07-01 Impact factor: 4.991
Authors: Tuuli H Suominen; Markku Alén; Timo Törmäkangas; Hans Degens; Jörn Rittweger; Ari Heinonen; Harri Suominen; Marko T Korhonen Journal: JBMR Plus Date: 2021-05-24