Interrelationship among muscle, fat, and bone: Connecting the dots on cellular, hormonal, and whole body levels

Ilich, Jasminka Z.; Kelly, Owen; Inglis, Julia Ellen; Panton, Lynn B.; Duque, Gustavo; Ormsbee, Michael J.

doi:10.1016/j.arr.2014.02.007

Cited by 218 publications

(219 citation statements)

References 115 publications

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“…However, inflammation may deregulate the MSC lineage commitment (11,31). Even under normal homeostatic conditions, MSC slightly favors adipogenic differentiation.…”

Section: The Detrimental Role Of Low-grade Chronic Inflammation In Obmentioning

confidence: 99%

“…Conversely, OPG, which is also produced by preosteoblasts, inhibits osteoclastogenesis by binding to RANKL, and thus promotes osteoblastogenesis. Upregulated pro-inflammatory cytokines, including TNF-α, IL-1, and IL-6 in obese state seem to mediate osteopenia and osteoporosis by regulating the RANKL/RANK/OPG pathway (31,35).…”

Section: Proposed Mechanism Of Actionmentioning

confidence: 99%

“…Since muscle and bone mass decline with age, and fat mass increases, it is possible that agerelated MSC lineage commitment dysfunction occurring in LGCI and coinciding with obesity causes both osteopenia (loss of bone) and sarcopenia (loss of muscle). For the extensive review on the connection between bone, muscle, and fat, see Ilich et al (31).…”

Section: The Detrimental Role Of Low-grade Chronic Inflammation In Obmentioning

confidence: 99%

“…For further review, see (11,31) are considered osteoresorptive. Both osteoblasts and adipocytes share MSC as their common precursor in the bone microenvironment.…”

Section: And Increases Cox-2 Expression Directly or Indirectly Via Thmentioning

confidence: 99%

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Low-grade chronic inflammation perpetuated by modern diet as a promoter of obesity and osteoporosis

Ilich

Kelly

Kim

et al. 2014

Archives of Industrial Hygiene and Toxicology

Self Cite

103

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Some of the universal characteristics of pre-agricultural hominin diets are strikingly different from the modern human diet. Hominin dietary choices were limited to wild plant and wild animal foods, while the modern diet includes more than 70 % of energy consumed from refined sugars, refined vegetable oils, and highly processed cereals and dairy products. The modern diet, with higher intake of fat has also resulted in a higher ratio of omega-6 (n-6) to omega-3 (n-3) polyunsaturated fatty acids (PUFA), contributing to low-grade chronic inflammation (LGCI) and thus promoting the development of many chronic diseases, including obesity and osteoporosis. In this review, we describe the changes in modern diet, focusing on the kind and amount of consumed fat; explain the shortcomings of the modern diet with regard to inflammatory processes; and delineate the reciprocity between adiposity and inflammatory processes, with inflammation being a common link between obesity and osteoporosis. We present the evidence that overconsumption of n-6 PUFA coupled with under-consumption of n-3 PUFA results in LGCI and, along with the increased presence of reactive oxygen species, leads to a shift in mesenchymal stem cells (precursors for both osteoblasts and adipocytes) lineage commitment toward increased adipogenesis and suppressed osteoblastogenesis. In turn, high n-6 to n-3 PUFA ratios in the modern diet, coupled with increased synthesis of pro-inflammatory cytokines due to adiposity, propagate obesity and osteoporosis by increasing or maintaining LGCI.

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“…However, inflammation may deregulate the MSC lineage commitment (11,31). Even under normal homeostatic conditions, MSC slightly favors adipogenic differentiation.…”

Section: The Detrimental Role Of Low-grade Chronic Inflammation In Obmentioning

confidence: 99%

Section: Proposed Mechanism Of Actionmentioning

confidence: 99%

Section: The Detrimental Role Of Low-grade Chronic Inflammation In Obmentioning

confidence: 99%

“…For further review, see (11,31) are considered osteoresorptive. Both osteoblasts and adipocytes share MSC as their common precursor in the bone microenvironment.…”

Section: And Increases Cox-2 Expression Directly or Indirectly Via Thmentioning

confidence: 99%

See 2 more Smart Citations

Low-grade chronic inflammation perpetuated by modern diet as a promoter of obesity and osteoporosis

Ilich

Kelly

Kim

et al. 2014

Archives of Industrial Hygiene and Toxicology

Self Cite

103

View full text Add to dashboard Cite

show abstract

“…Beyond the profound influence on systemic aging and body metabolism, muscle secrete myokines, which act on muscles and other tissues, such as adipose, bones and brain in an autocrine, paracrine, and endocrine fashion [61]. The metabolites released from muscle and the interactions between muscle and nerve also participate in the systemic effects of muscle on the organism's physiology.…”

Section: Sarcopenia Accelerates Systemic Aging Frailty and Age-relamentioning

confidence: 99%

From Sarcopenia to Frailty: The Pathophysiological Basis and Potential Target Molecules of Intervention

Yu¹,

Ruan²,

Greco³

2017

Frailty and Sarcopenia - Onset, Development and Clinical Challenges

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Skeletal muscle is not only an endocrine organ but also one of core components of muscloskeletal system. Sarcopenia refers to a decline in the skeletal muscle mass and function. The former involves the size and number of changes in two types of myofibers, lower satellite cell density, and regeneration ability. The latter shows a loss of muscle strength. Frailty is a geriatric syndrome with multisystem impairment associated with increased vulnerability to stressors. Sarcopenia increases the risk of frailty and may be one of the major causes of physical frailty phenotype. Sarcopenia is also potentially associated with cognitive frailty phenotype. Aging might be the common underlying pathophysiology of sarcopenia and frailty. Therefore, there are some potential target molecules in aging-related signaling pathways that might be associated with sarcopenia and frailty. Nevertheless, sarcopenia can mediate metabolism and promote accelerate systemic aging, frailty, and age-related diseases by myokines in an endocrine manner. Lifestyle interventions (resistance exercise and dietary restriction) of gerontoscience are effective in the prevention of sarcopenia. Some pharmacological agents are registered in different phases of clinical trials for sarcopenia intervention. Phytochemicals, mTOR inhibitors, metformin and acarbose, NAD precursors, and sirtuin activators demonstrated that multiple target antiaging effects might also have preventive and therapeutic perspectives on sarcopenia and frailty.

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Sarcopenia and Osteoporosis

Duque

Binkley

2018

Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism

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Interrelationship among muscle, fat, and bone: Connecting the dots on cellular, hormonal, and whole body levels

Cited by 218 publications

References 115 publications

Low-grade chronic inflammation perpetuated by modern diet as a promoter of obesity and osteoporosis

Low-grade chronic inflammation perpetuated by modern diet as a promoter of obesity and osteoporosis

From Sarcopenia to Frailty: The Pathophysiological Basis and Potential Target Molecules of Intervention

Sarcopenia and Osteoporosis

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