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Cited by 510Muscle Physiology and DisordersExercise and Physiological ResponsesAdipokines, Inflammation, and Metabolic Diseases

Muscle, Bone, and Fat Crosstalk: The Biological Role of Myokines, Osteokines, and Adipokines

Kirk, Ben, Feehan, Jack, Lombardi, Giovanni, Duque, Gustavo·2020·Current Osteoporosis Reports
DOI 10.1007/s11914-020-00599-y
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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.

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  • Exercise-responsive myokines participate in muscle-bone crosstalk and regulate exercise-associated bone remodeling, whereas chronic inflammatory signaling in wasting or inflammatory states may shift bone remodeling toward impaired bone formation and enhanced resorption.

    “Exercise-responsive myokines participate in muscle–bone crosstalk and regulate exercise-associated bone remodeling, whereas chronic inflammatory signaling in wasting or inflammatory states may shift bone remodeling toward impaired bone formation and enhanced resorption [51]”

    From Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies (2026) · cites this paper as [51]

  • Exercise triggers release of exerkines, which contribute to increased muscle anabolism, bone formation, mitochondrial function, glucose utilization, and fatty acid oxidation, ultimately alleviating sarcopenia.

    “exercise triggers the release of bioactive factors known as exerkines, which contribute to increased muscle anabolism, bone formation, mitochondrial function, glucose utilization, and fatty acid oxidation (FAO), ultimately alleviating sarcopenia [72].”

    From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [72]

  • In muscle aging, increased plasma levels of IL-6 and TNF-α, associated with loss of muscle strength, activate cell signaling pathways that lead to skeletal muscle atrophy.

    “In muscle aging, increased plasma levels of IL-6 and TNF-α, associated with loss of muscle strength, activate cell signaling pathways that lead to skeletal muscle atrophy, which in turn induce resistance to IL-6, a condition that shares similarities with insulin or leptin resistance [98].”

    From Adipokines, Myokines, and Hepatokines: Crosstalk and Metabolic Repercussions (2021) · cites this paper as [98]

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Authors
Kirk, B., Feehan, J., Lombardi, G., & Duque, G.
Affiliations
  • The University of Melbourne (AU)
  • IRCCS Ospedale Galeazzi - Sant'Ambrogio (IT)
Corresponding author
Duque, Gustavo
ORCID
Venue
Current Osteoporosis Reports
Publisher
Springer Science and Business Media LLC
Published
2020-06-12
Volume
18
Issue
4
Pages
388-400
ISSN
  • 1544-1873 (ISSN-L)
  • 1544-2241
DOI
10.1007/s11914-020-00599-y
OpenAlex
W3034508206
Cited by
510
References
145
Citations by year
2026: 82 · 2025: 98 · 2024: 87 · 2023: 102 · 2022: 72 · 2021: 61 · 2020: 8
FWCI
5.82
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Current Osteoporosis Reports (publishedVersion)
  • PubMed (publishedVersion)
  • Victoria University Research Repository (Victoria University) (submittedVersion)
Funders
Australian Institute for Musculoskeletal Science (N/A)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
myokines, osteokines, adipokines, mechanotransduction, interleukin-6, irisin, insulin-like growth factor I, brain-derived neurotrophic factor, myostatin, osteocalcin, sclerostin, leptin, resistin, adiponectin, TNF-α, adipose tissue browning, thermogenesis, low-grade inflammation, physical activity, muscle anabolism, bone formation, mitochondrial biogenesis, aging
MeSH terms
Adipose Tissue, Organelle Biogenesis, Bone and Bones, Energy Intake, Fatty Acids, Fibronectins, Glucose, Humans, Inflammation, Insulin-Like Growth Factor I, Osteogenesis, Oxidation-Reduction, Tumor Necrosis Factor-alpha, Exercise, Osteocalcin, Interleukin-6, Fibroblast Growth Factor 2, Muscle, Skeletal, Brain-Derived Neurotrophic Factor, Autocrine Communication, Paracrine Communication, Adaptor Proteins, Signal Transducing, Leukemia Inhibitory Factor, Adipokines, Myostatin

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