Associations between lean mass and leptin in men with chronic spinal cord injury: Results from the FRASCI-muscle study

Park, Andrew J; Battaglino, Ricardo A.; Nguyen, Nguyen M H; Morse, Leslie R.

doi:10.1371/journal.pone.0198969

Cited by 12 publications

(11 citation statements)

References 48 publications

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“…Exercise and diet have been reported to improve gait speed and leptin ( 87 ). One study reported that exercise affects the balance of pro-inflammatory cytokines such as leptin ( 88 ). Sarcopenic obesity markers such as IGF-1, leptin, and adiponectin improve significantly after 16 weeks of endurance and resistance exercise compared to usual care ( 10 , 25 ).…”

Section: Leptinmentioning

confidence: 99%

Exercise Therapy for People With Sarcopenic Obesity: Myokines and Adipokines as Effective Actors

Pahlavani

2022

Front. Endocrinol.

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Sarcopenic obesity is defined as a multifactorial disease in aging with decreased body muscle, decreased muscle strength, decreased independence, increased fat mass, due to decreased physical activity, changes in adipokines and myokines, and decreased satellite cells. People with sarcopenic obesity cause harmful changes in myokines and adipokines. These changes are due to a decrease interleukin-10 (IL-10), interleukin-15 (IL-15), insulin-like growth factor hormone (IGF-1), irisin, leukemia inhibitory factor (LIF), fibroblast growth factor-21 (FGF-21), adiponectin, and apelin. While factors such as myostatin, leptin, interleukin-6 (IL-6), interleukin-8 (IL-8), and resistin increase. The consequences of these changes are an increase in inflammatory factors, increased degradation of muscle proteins, increased fat mass, and decreased muscle tissue, which exacerbates sarcopenia obesity. In contrast, exercise, especially strength training, reverses this process, which includes increasing muscle protein synthesis, increasing myogenesis, increasing mitochondrial biogenesis, increasing brown fat, reducing white fat, reducing inflammatory factors, and reducing muscle atrophy. Since some people with chronic diseases are not able to do high-intensity strength training, exercises with blood flow restriction (BFR) are newly recommended. Numerous studies have shown that low-intensity BFR training produces the same increase in hypertrophy and muscle strength such as high-intensity strength training. Therefore, it seems that exercise interventions with BFR can be an effective way to prevent the exacerbation of sarcopenia obesity. However, due to limited studies on adipokines and exercises with BFR in people with sarcopenic obesity, more research is needed.

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Section: Leptinmentioning

confidence: 99%

Exercise Therapy for People With Sarcopenic Obesity: Myokines and Adipokines as Effective Actors

Pahlavani

2022

Front. Endocrinol.

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“…Moreover, sarcopenic individuals exhibit lower leptin titers [84]. Seeing as leptin receptors are abundant in skeletal muscles, it has been stated that leptin may regulate metabolic activity at this level [85,86]. Nonetheless, while classically considered a mainly pro-inflammatory adipokine, leptin may also be released by skeletal muscles, thus becoming an adipomyokine.…”

Section: Skeletal Muscle and White Adipose Tissue In Old Age: Acomplex Relationshipmentioning

confidence: 99%

“…Several pathological conditions are associated with sedentary behavior, sarcopenia, and increased fat mass. Leptin levels have been shown to be increased in patients with spinal cord injuries [85]. Yet sarcopenic older subject demonstrates lower leptin concentrations [84].…”

Section: Skeletal Muscle and White Adipose Tissue In Old Age: Acomplex Relationshipmentioning

confidence: 99%

Inactivity and Skeletal Muscle Metabolism: A Vicious Cycle in Old Age

Rezuş

Burlui

Cardoneanu

et al. 2020

IJMS

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Aging is an inevitable and gradually progressive process affecting all organs and systems. The musculoskeletal system makes no exception, elderly exhibit an increased risk of sarcopenia (low muscle mass),dynapenia (declining muscle strength), and subsequent disability. Whereas in recent years the subject of skeletal muscle metabolic decline in the elderly has been gathering interest amongst researchers, as well as medical professionals, there are many challenges yet to be solved in order to counteract the effects of aging on muscle function efficiently. Noteworthy, it has been shown that aging individuals exhibit a decline in skeletal muscle metabolism, a phenomenon which may be linked to a number of predisposing (risk) factors such as telomere attrition, epigenetic changes, mitochondrial dysfunction, sedentary behavior (leading to body composition alterations), age-related low-grade systemic inflammation (inflammaging), hormonal imbalance, as well as a hypoproteic diet (unable to counterbalance the repercussions of the age-related increase in skeletal muscle catabolism). The present review aims to discuss the relationship between old age and muscle wasting in an effort to highlight the modifications in skeletal muscle metabolism associated with aging and physical activity.

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“…SCI was confirmed by physical examination by a trained rater according to the American Spinal Injury Association Impairment Scale (AIS) as previously described. 14,15 Peripheral blood mononuclear cells isolation Approximately 30 mL of peripheral blood extracted from each participant were drawn into a heparinized tube and diluted at a ratio of 1:2 with phosphate-buffered saline (PBS) solution. The wholeblood PBS solution was layered onto one volume of Histopaque Ò -1077 (Sigma-Aldrich, St. Louis, MO).…”

Section: Spinal Cord Injury Classificationmentioning

confidence: 99%

TMEM176A and TMEM176B Are Candidate Regulators of Inhibition of Dendritic Cell Maturation and Function after Chronic Spinal Cord Injury

Picotto

Morse

Nguyen

et al. 2020

Journal of Neurotrauma

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Inhibition of dendritic cell maturation and activation, together with abnormal functioning of cell-mediated immunity, has been reported in chronic spinal cord injury (SCI). The development of immune-based therapies could: 1) prevent or slow down limit further tissue damage in chronic SCI, and 2) promote tissue regeneration. To identify novel candidate molecular pathways mediating SCI-induced immune changes, we performed whole-genome microarray and molecular pathway analyses. Subjects with motor complete chronic SCI (> 2 years post-injury) and uninjured controls were selected from an ongoing study. Microarray analysis was performed with RNA extracted from circulating monocytes. Partek Genomic Suite (PGS) software was used to limit the 54,000 gene list to only those genes up-regulated or down-regulated by 2-fold or more in SCI compared with control. Pathway analyses were performed with Ingenuity Systems IPA software to identify biological pathways of interest involving differentially expressed genes. Genes of interest were then confirmed by quantitative PCR (qPCR). Six SCI subjects and five uninjured controls were included in the final analyses. A molecular pathway related to immune cell trafficking was identified as being significantly upregulated in the SCI subjects. Two genes in that network, transmembrane domain protein (TMEM)176A and TMEM176B, were notable for the magnitude of overexpression. Dendritic cells have been shown to mediate recovery and/or protective autoimmunity in central nervous system injuries and have the capacity to induce neuroprotection and neurogenesis in stroke patients. High TMEM176A and TMEM176B levels have been shown to prevent dendritic cell maturation and inhibit dendritic cell activity in the general population. Here, we report overexpression of both genes in SCI compared with control subjects. Thus, we propose that TMEM176A and TMEM176B are candidate genes involved in inhibiting protective immune responses in SCI. This study may support future research aimed at developing new targets for therapies to promote immune systemmediated neuroprotection and recovery in SCI.

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Associations between lean mass and leptin in men with chronic spinal cord injury: Results from the FRASCI-muscle study

Cited by 12 publications

References 48 publications

Exercise Therapy for People With Sarcopenic Obesity: Myokines and Adipokines as Effective Actors

Exercise Therapy for People With Sarcopenic Obesity: Myokines and Adipokines as Effective Actors

Inactivity and Skeletal Muscle Metabolism: A Vicious Cycle in Old Age

TMEM176A and TMEM176B Are Candidate Regulators of Inhibition of Dendritic Cell Maturation and Function after Chronic Spinal Cord Injury

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