The relationship between plasma interleukin-15 levels and sarcopenia in outpatient older people

Yalçın, Ahmet; Sılay, Kamile; Balık, Ahmet Rıfat; Avcıoğlu, Gamze; Aydin, Almila Senat

doi:10.1007/s40520-017-0848-y

Cited by 43 publications

(24 citation statements)

References 27 publications

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“…IL-15 levels are increased by exercise in humans (Rinnov et al, 2014 ). On the other skeletal muscle aging and sarcopenia are associated with low levels of IL-15 (Yalcin et al, 2018 ). Here, we show that exercise reduced IL-15 mRNA level in aged control and Nmrk2 −/− mice.…”

Section: Discussionmentioning

confidence: 99%

Aged Nicotinamide Riboside Kinase 2 Deficient Mice Present an Altered Response to Endurance Exercise Training

et al. 2018

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Background: Skeletal muscle aging is marked by the development of a sarcopenic phenotype, a global decline of muscle energetic capacities, and an intolerance to exercise. Among the metabolic disorders involved in this syndrome, NAD metabolism was shown to be altered in skeletalmuscle, with an important role for the NAMPT enzyme recycling the nicotinamide precursor. An alternative pathway for NAD biosynthesis has been described for the nicotinamide riboside vitamin B3 precursor used by the NMRK kinases, including the striated muscle-specific NMRK2.Aim: With this study, our goal is to explore the ability of 16-month-old Nmrk2−/− mice to perform endurance exercise and study the consequences on muscle adaptation to exercise.Methods: 10 control and 6 Nmrk2−/− mice were used and randomly assigned to sedentary and treadmill endurance training groups. After 9 weeks of training, heart and skeletal muscle samples were harvested and used for gene expression analysis, NAD levels measurements and immunohistochemistry staining.Results: Endurance training triggered a reduction in the expression of Cpt1b and AcadL genes involved in fatty acid catabolism in the heart of Nmrk2−/− mice, not in control mice. NAD levels were not altered in heart or skeletal muscle, nor at baseline neither after exercise training in any group. Myh7 gene encoding for the slow MHC-I was more strongly induced by exercise in Nmrk2−/− mice than in controls. Moreover, IL-15 expression levels is higher in Nmrk2−/− mice skeletal muscle at baseline compared to controls. No fiber type switch was observed in plantaris after exercise, but fast fibers diameter was reduced in aged control mice, not in Nmrk2−/− mice. No fiber type switch or diameter modification was observed in soleus muscle.Conclusion: In this study, we demonstrated for the first time a phenotype in old Nmrk2−/− mice in response to endurance exercise training. Although NMRK2 seems to be predominantly dispensable to maintain global NAD levels in heart and skeletal muscle, we demonstrated a maladaptive metabolic response to exercise in cardiac and skeletal muscle, showing that NMRK2 has a specific and restricted role in NAD signaling compared to the NAMPT pathway.

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Section: Discussionmentioning

confidence: 99%

Aged Nicotinamide Riboside Kinase 2 Deficient Mice Present an Altered Response to Endurance Exercise Training

et al. 2018

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“…However, IL-15 receptor signalling subunit IL2RB expression was 80% lower in older muscle, suggesting that the intracellular promyogenic effects of IL-15 may be blunted in the elderly. In a separate study, plasma IL-15 concentrations were found to be lower in sarcopenic compared to nonsarcopenic older adults and inversely correlated with sarcopenic state and body mass index (BMI) [50]. With regard to adiposity and IL-15 expression, obese individuals present with lower serum IL-15 than normal-weight individuals and IL-15 knockout in mice results in weight gain [139].…”

Section: Interleukin-15mentioning

confidence: 95%

Recent advances and future avenues in understanding the role of adipose tissue cross talk in mediating skeletal muscle mass and function with ageing

2021

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Sarcopenia, broadly defined as the age-related decline in skeletal muscle mass, quality, and function, is associated with chronic low-grade inflammation and an increased likelihood of adverse health outcomes. The regulation of skeletal muscle mass with ageing is complex and necessitates a delicate balance between muscle protein synthesis and degradation. The secretion and transfer of cytokines, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), both discretely and within extracellular vesicles, have emerged as important communication channels between tissues. Some of these factors have been implicated in regulating skeletal muscle mass, function, and pathologies and may be perturbed by excessive adiposity. Indeed, adipose tissue participates in a broad spectrum of inter-organ communication and obesity promotes the accumulation of macrophages, cellular senescence, and the production and secretion of pro-inflammatory factors. Pertinently, age-related sarcopenia has been reported to be more prevalent in obesity; however, such effects are confounded by comorbidities and physical activity level. In this review, we provide evidence that adiposity may exacerbate age-related sarcopenia and outline some emerging concepts of adipose-skeletal muscle communication including the secretion and processing of novel myokines and adipokines and the role of extracellular vesicles in mediating inter-tissue cross talk via lncRNAs and miRNAs in the context of sarcopenia, ageing, and obesity. Further research using advances in proteomics, transcriptomics, and techniques to investigate extracellular vesicles, with an emphasis on translational, longitudinal human studies, is required to better understand the physiological significance of these factors, the impact of obesity upon them, and their potential as therapeutic targets in combating muscle wasting.

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“…In the mice muscle and serum, IL-15 protein levels decline progressively with advanced age (Quinn et al, 2010). Further, Yalcin et al (2018) demonstrated that the level of IL-15 is significantly lower in patients with sarcopenia compared to non-sarcopenic old people. A study conducted on a C2C12 muscle cell line presented the protective effects of IL-15 against H 2 O 2 -iduced oxidative stress.…”

Section: Endocrine Function Of the Skeletal Muscle And Neurodegenerationmentioning

confidence: 96%

Iron Metabolism of the Skeletal Muscle and Neurodegeneration

et al. 2019

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Recent studies clearly indicate that the endocrine function of the skeletal muscle is essential for a long and healthy life. Regular exercise, which has been shown to stimulate the release of myokines, lowers the risk of many diseases, including Alzheimer’s and Parkinson’s disease, emphasizing the role of skeletal muscle in proper functioning of other tissues. In addition, exercise increases insulin sensitivity, which may also impact iron metabolism. Even though the role of iron in neurodegeneration is well established, the exact mechanisms of iron toxicity are not known. Interestingly, exercise has been shown to modulate iron metabolism, mainly by reducing body iron stores. Insulin signaling and iron metabolism are interconnected, as high tissue iron stores are associated with insulin resistance, and conversely, impaired insulin signaling may lead to iron accumulation in an affected tissue. Excess iron accumulation in tissue triggers iron-dependent oxidative stress. Further, iron overload in the skeletal muscle not only negatively affects muscle contractility but also might impact its endocrine function, thus possibly affecting the clinical outcome of diseases, including neurodegenerative diseases. In this review, we discuss possible mechanisms of iron dependent oxidative stress in skeletal muscle, its impact on muscle mass and endocrine function, as well as on neurodegeneration processes.

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The relationship between plasma interleukin-15 levels and sarcopenia in outpatient older people

Abstract: A low level of plasma IL-15 is associated with sarcopenia in outpatient older people. Further longitudinal and prospective studies are needed to evaluate changes in IL-15 over time together with muscle mass and strength or therapeutic potential of IL-15.

Cited by 43 publications

References 27 publications

Aged Nicotinamide Riboside Kinase 2 Deficient Mice Present an Altered Response to Endurance Exercise Training

Aged Nicotinamide Riboside Kinase 2 Deficient Mice Present an Altered Response to Endurance Exercise Training

Recent advances and future avenues in understanding the role of adipose tissue cross talk in mediating skeletal muscle mass and function with ageing

Iron Metabolism of the Skeletal Muscle and Neurodegeneration

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