• NAD+
• NAMPT
• T2DM
• aging
• skelelal muscle

• Mendelian randomization
• appendicular lean mass
• circulating cytokines
• grip strength
• inflammatory cytokines
• sarcopenia

• Humans
• Mendelian Randomization Analysis
• Sarcopenia/blood
• Sarcopenia/genetics
• Cytokines/blood
• Cytokines/genetics
• Polymorphism, Single Nucleotide
• Genome-Wide Association Study
• Hand Strength

• 24NDQN156YBM Zhejiang Federation of Humanities and Social Sciences
• Y202248649 Scientific Research Fund of Zhejiang Provincial Education Department

• Blood factors
• CHARLS
• Muscle weakness
• Sarcopenia

• Humans
• Sarcopenia/blood
• Sarcopenia/epidemiology
• Sarcopenia/diagnosis
• Male
• China/epidemiology
• Female
• Longitudinal Studies
• Aged
• Independent Living/statistics & numerical data
• C-Reactive Protein/analysis
• Middle Aged
• Cross-Sectional Studies
• Glycated Hemoglobin/analysis
• Blood Urea Nitrogen
• Retirement
• Risk Factors
• Logistic Models

• Correlation
• Liver cancer
• Nutritional risk index
• Prognosis
• Radical resection
• Systemic immune inflammation index

• elderly
• muscle strength
• sarcopenia
• thyroid hormone

• Humans
• Aged
• Aged, 80 and over
• Hand Strength
• Thyroid Hormones
• Sarcopenia/epidemiology
• Muscle Strength
• Thyrotropin

• National Natural Science Foundation of China

• imbalance of protein synthesis and breakdown
• molecular mechanism
• neuromuscular junction lesion
• sarcopenia
• satellite cells dysfunction

• Intrinsic capacity
• older adults
• sarcopenia

• Humans
• Male
• Female
• Aged
• Cross-Sectional Studies
• Sarcopenia
• Geriatric Assessment
• Cognition
• Hand Strength/physiology
• Hospitalization
• Aged, 80 and over
• Middle Aged
• Gait
• Walking Speed

• locally advanced gastric cancer
• marker
• prognostic nutritional index
• sarcopenia
• systemic immune-inflammatory index

Background: In patients with chronic kidney disease (CKD), there is an overproduction and accumulation of advanced glycation end-products (AGEs). Since AGEs may have detrimental effects on muscular trophism and performance, we evaluated whether they may contribute to the onset of sarcopenia in CKD patients. Methods: We enrolled 117 patients. The AGEs were quantified by fluorescence intensity using a fluorescence spectrophotometer and soluble receptor for AGE (sRAGE) isoforms by ELISA. As for the sarcopenia definition, we used the European Working Group on Sarcopenia in Older People (EWGSOP2) criteria. Results: The average age was 80 ± 11 years, 70% were males, and the mean eGFR was 25 + 11 mL/min/1.73 m². Sarcopenia was diagnosed in 26 patients (with a prevalence of 22%). The sarcopenic patients had higher levels of circulating AGEs (3405 ± 951 vs. 2912 ± 722 A.U., p = 0.005). AGEs were higher in subjects with a lower midarm muscle circumference (MAMC) (3322 ± 919 vs. 2883 ± 700 A.U., respectively; p = 0.005) and were directly correlated with the gait test time (r = 0.180, p = 0.049). The total sRAGE and its different isoforms (esRAGE and cRAGE) did not differ in patients with or without sarcopenia. Conclusions: In older CKD patients, AGEs, but not sRAGE, are associated with the presence of sarcopenia. Therefore, AGEs may contribute to the complex pathophysiology leading to the development of sarcopenia in CKD patients.

Background: Chronic inflammation is a pathophysiological cause of sarcopenia in Crohn’s disease (CD) patients. However, the potential impact of diet-related inflammation on sarcopenia has not yet been adequately investigated. We examined the associations between Dietary Inflammatory Index (DII) and sarcopenia in CD patients. Methods: A total of 140 CD patients from Ruijin Hospital in Shanghai were included in this cross-sectional study. DII scores were calculated from the dietary data collected using a validated food frequency questionnaire (FFQ). Sarcopenia was determined according to the Asian Working Group for Sarcopenia. Multivariable logistic regression analyses were performed to determine the association between DII and sarcopenia. Results: The mean DII score was 0.81 ± 2.13, ranging from −3.24 to 4.89. The overall prevalence of sarcopenia was 26.4%. The higher DII score significantly increased the risk of sarcopenia in CD patients (OR_Quartile4vs1: 9.59, 95% CI: 1.69, 54.42, p_trend = 0.031) in the multivariable model after adjusting for more potential confounders. Moreover, CD patients with a lower DII had a significantly higher appendicular skeletal muscle mass index (ASMI, OR_Quartile4vs1: 5.48, 95% CI: 1.51, 19.87, p_trend = 0.018) after adjusting for age, gender, BMI, smoking status and drinking status model. Yet, there were no significant differences between DII and ASMI after adjusting for more potential confounders. Additionally, no significant association was observed between DII and handgrip strength in the multivariable-adjusted models. Conclusions: Pro-inflammatory diet was associated with increased risk of sarcopenia in CD patients. CD patients should have a proper intake of energy and protein. These patients could also benefit from supplementation with enteral nutrition due to its anti-inflammatory potential.

• Crohn’s disease
• dietary inflammatory index
• malnutrition
• sarcopenia

We aimed to explore the potential association of body composition parameters measured by bioelectrical impedance analysis (BIA) with the incidence of sarcopenia in patients with acute myeloid leukemia (AML) (non-M3) after chemotherapy.

This was a single-center observational study. Sixty-nine patients with newly diagnosed AML underwent BIA at the time of initial diagnosis and after completion of three chemotherapy sessions. Pre- and post-chemotherapy BIA parameters were compared. Sarcopenia was defined as low skeletal muscle mass plus low muscle strength according to the Asian Working Group for Sarcopenia (AWGS). Association of sarcopenia with mid-arm muscle circumference (MAMC) and intracellular water (ICW) was assessed by multivariate logistic regression.

There was a significant increase in the prevalence of sarcopenia after chemotherapy (39.1% vs 14.5%, P<0.001). Skeletal muscle mass (SMM), fat-free mass (FFM), and soft lean mass (SLM) showed a significant decrease after chemotherapy (P<0.05). MAMC, ICW, and total body water (TBW) significantly decreased after chemotherapy (P<0.05). BIA indices including appendicular skeletal muscle mass (ASM) (r=0.889, P<0.001), ICW (r=0.869, P<0.001), MAMC (r=0.849, P<0.001) showed a positive correlation with SMI. Moreover, ASM (r=−0.453 P=0.001), ICW (r=−0.322, P<0.05), and MAMC (r=−0.352, P<0.05) showed a negative correlation with sarcopenia. On multivariate logistic regression analysis, increased ICW was associated with decreased risk of sarcopenia [odds ratio (OR): 0.50; 95% confidence interval (CI) 0.30–0.82]. Each additional unit of MAMC after chemotherapy was associated with 71% lower risk of sarcopenia (OR: 0.29; 95% CI 0.13–0.66).

The incidence of sarcopenia was associated with chemotherapy of patients with AML (non-M3) as reflected by body composition changes.

Aging promotes most degenerative pathologies in mammals, which are characterized by progressive decline of function at molecular, cellular, tissue, and organismal levels and account for a host of health care expenditures in both developing and developed nations. Sarcopenia is a prominent age-related disorder in musculoskeletal system. Defined as gradual and generalized chronic skeletal muscle disorder, sarcopenia involves accelerated loss of muscle mass, strength and function, which is associated with increased adverse functional outcomes and evolutionally refers to muscle wasting accompanied by other geriatric syndromes. More efforts have been made to clarify mechanisms underlying sarcopenia and new findings suggest that it may be feasible to delay age-related sarcopenia by modulating fundamental mechanisms such as cellular senescence. Cellular senescence refers to the essentially irreversible growth arrest mainly regulated by p53/p21^CIP1 and p16^INK4a/pRB pathways as organism ages, possibly detrimentally contributing to sarcopenia via muscle stem cells (MuSCs) dysfunction and the senescence-associated secretory phenotype (SASP) while cellular senescence may have beneficial functions in counteracting cancer progression, tissue regeneration and wound healing. By now diverse studies in mice and humans have established that targeting cellular senescence is a powerful strategy to alleviating sarcopenia. However, the mechanisms through which senescent cells contribute to sarcopenia progression need to be further researched. We review the possible mechanisms involved in muscle stem cells (MuSCs) dysfunction and the SASP resulting from cellular senescence, their associations with sarcopenia, current emerging therapeutic opportunities based on targeting cellular senescence relevant to sarcopenia, and potential paths to developing clinical interventions genetically or pharmacologically.

• aging
• cellular senescence
• muscle stem cells (MuSCs) dysfunction
• sarcopenia
• senescence-associated secretory phenotype (SASP)

Accumulating research indicates that handgrip strength is associated with cognitive function. Studies have also shown the difference in cognitive decline between males and females. We investigated the association between baseline handgrip strength and later cognitive function in older adults according to sex using the dataset from Korean Longitudinal Study of Aging (2006–2018). Overall, 9707 observations of 1750 participants (989 males and 761 females) over 65 years of age were sampled from the first wave, followed by six consecutive waves. The Korean version of the Mini-Mental State Examination and baseline handgrip strength scores were assessed. Sociodemographic and health-related variables were also included as covariates in the multivariable linear mixed models. Males in the lowest quartile of the baseline handgrip strength decreased in cognitive function (β = −0.54, standard error (SE) = 0.16, p < 0.001), compared to males in the highest quartile. For females, those in the second lowest quartile (β = −0.65, SE = 0.19, p < 0.001) and the lowest quartile (β = −0.53, SE = 0.19, p< 0.01) decreased in cognitive function. Handgrip strength may be positively associated with later cognitive function, but the association may be non-linear and differ between sexes. Sex-specific preventive assessment of handgrip strength may help identify older adults at risk for cognitive impairment.

• KLoSA
• South Korea
• aging
• cognitive decline
• handgrip strength
• physical strength

Although skeletal muscle is the main effector organ largely accounting for disability after stroke, considerably less attention is paid to the secondary abnormalities of stroke-related skeletal muscle loss. It is necessary to explore the mechanism of muscle atrophy after stroke and further develop effective rehabilitation strategy. Here, we evaluated the effects of high-intensity interval (HIIT) versus moderate-intensity aerobic training (MOD) on physical function, muscle mass, and stroke-related gene expression profile of skeletal muscle. After the model of middle cerebral artery occlusion (MCAO) was successfully made, the blood lactate threshold corresponding speed (S_LT) and maximum speed (S_max) were measured. Different intensity training protocols (MOD < S_LT; S_LT < HIIT < S_max) were carried out for 3 weeks beginning at 7 days after MCAO in the MOD and HIIT groups, respectively. We found that both HIIT and MOD prevented stroke-related gastrocnemius muscle mass loss in MCAO mice. HIIT was more beneficial than MOD for improvements in muscle strength, motor coordination, walking competency, and cardiorespiratory fitness. Furthermore, HIIT was superior to MOD in terms of reducing lipid accumulation, levels of IL-1β and IL-6 in paretic gastrocnemius, and improving peripheral blood CD4+/CD8+ T cell ratio, level of IL-10. Additionally, RNA-seq analysis revealed that the differentially expressed genes among HIIT, MOD, and MCAO groups were highly associated with signaling pathways involved in inflammatory response, more specifically the I-kappaB kinase/NF-kappaB signaling. Following the outcome, we further investigated the infiltrating immune cells abundant in paretic muscles. The results showed that HIIT modulated macrophage activation by downregulating CD86+ (M1 type) macrophages and upregulating CD163+ (M2 type) macrophages via inhibiting the TLR4/MyD88/NFκB signaling pathway and exerting an anti-inflammatory effect in paretic skeletal muscle. It is expected that these data will provide novel insights into the mechanisms and potential targets underlying muscle wasting in stroke.

• dietary pattern
• grip strength
• middle‐aged adults
• muscle strength

• Kermanshah University of Medical Sciences

• aging
• muscle growth
• nutrition
• sarcopenia
• seafood

• aging
• chronic low-grade inflammation
• frailty
• gut microbiota
• review

Background: Sarcopenia contributes to increased morbidity and mortality in patients undergoing surgery for abdominal aortic aneurysms (AAA). However, few reports have demonstrated whether sarcopenia would affect the development of postoperative acute kidney injury (AKI) in these patients. This study aimed to examine whether sarcopenia is associated with AKI and morbidity and mortality after infrarenal AAA operation. Methods: We retrospectively analysed 379 patients who underwent infrarenal AAA surgery. The diagnosis of sarcopenia was performed using the skeletal muscle index, which was calculated from axial computed tomography at the level of L3. The patients were separated into those with sarcopenia (n = 104) and those without sarcopenia (n = 275). We applied multivariable and Cox regression analyses to evaluate the risk factors for AKI and overall mortality. A propensity score matching (PSM) evaluation was done to assess the postoperative results. Results: The incidence of AKI was greater in sarcopenia than non-sarcopenia group before (34.6% vs. 15.3%; p < 0.001) and after the PSM analysis (34.6% vs. 15.4%; p = 0.002). Multivariable analysis revealed sarcopenia to be associated with AKI before (p = 0.010) and after PSM (p = 0.016). Sarcopenia was also associated with overall mortality before (p = 0.048) and after PSM (p = 0.032). A Kaplan–Meier analysis revealed that overall mortality was elevated patients with sarcopenia before and after PSM than in those without (log-rank test, p < 0.001, p = 0.022). Conclusions: Sarcopenia was associated with increased postoperative AKI incidence and overall mortality among individuals who underwent infrarenal AAA operation.

• abdominal aortic aneurysm
• acute kidney injury
• postoperative outcome
• sarcopenia

• food-based inflammatory potential of the diet
• gait speed
• muscle mass
• muscle strength
• sarcopenia

Sarcopenia is a multifaceted geriatric syndrome associated with the loss of muscle mass. We examined the relationship between low muscle mass and inflammatory cytokines in the context of aging. This study involved 299 participants (127 men and 172 women; mean age 63.3 ± 9.8 years) who underwent health checkups for body composition and inflammatory cytokine (TNF-alpha, IL-6, and MCP-1) levels. Muscle mass was determined using the skeletal muscle mass index. We divided the participants into the normal (N) and low muscle mass (L) groups and compared the levels of inflammatory cytokines in nonelderly (<65 years) and elderly (≥65 years) participants. Among the nonelderly subjects, C-reactive protein was significantly lower in the L group than in the N group (p < 0.05). However, there was no significant difference in the inflammatory cytokine levels between the groups. Among the elderly subjects, the TNF-alpha level was significantly lower in the L group than in the N group (p < 0.05), whereas there were no significant differences in the IL-6 and MCP-1 levels. Moreover, TNF-alpha was identified as a risk factor for the L group in the logistic regression analysis (Exp (B) 0.935, 95% CI: 0.876–0.997, p = 0.04). Although a low TNF-alpha level is a risk factor for low muscle mass, inflammatory cytokine levels are not necessarily elevated in elderly individuals with the loss of muscle mass.

sarcopenia is a highly prevalent condition in elderly individuals which is characterized by loss of muscle mass and functions; recent results showed that it is also associated with inflammation. Rehabilitation protocols for sarcopenia are designed to improve physical conditions, but very scarce data are available on their effects on inflammation We verified whether in sarcopenic patients the inflammation is reduced by rehabilitation and investigated the biological correlates of such effect.

Twenty-one sarcopenic patients undergoing a specifically-designed rehabilitation program were enrolled in the study. Physical, cognitive and nutritional parameters, as well as the concentration of C-Reactive Protein (CRP), pro-and anti-inflammatory cytokines and cytokine production-modulating miRNAs were measured at the beginning (T₀) and at end (30-days; T₁) of the rehabilitation.

Rehabilitation resulted in a significant improvement of physical and cognitive conditions; this was accompanied by a significant reduction of CRP (p = 0.04) as well as of IL-18 (p = 0.008) and IL-37 (p = 0.009) concentration. Notably, the concentration of miR-335-3p (p = 0.007) and miR-657, the two known post-transcriptional regulators of IL-37 production, was increased by the rehabilitation protocol.

Results herein confirm that successful rehabilitation for sarcopenia results in a reduction of the inflammatory milieu, raise the possibility that IL-37 may be a key target to monitor the rehabilitation-associated improvement in sarcopenia, and suggest that this cytokine could be a therapeutic target in sarcopenic patients.

• Cytokines
• IL-37
• Inflammaging
• MiRNAs
• Rehabilitation
• Sarcopenia

Nutrition has an important impact on inflammatory bowel diseases (IBD). In particular, several studies have addressed its role in their pathogenesis, showing how the incidence of IBD significantly increased in recent years. Meanwhile, nutrition should be considered a component of the treatment of the disease, both as a therapy itself, and especially in the perspective of correcting the various nutritional deficiencies shown by these patients. In this perspective, nutritional suggestions are very important even in the most severe forms of IBD, requiring hospitalization or surgical treatment. Although current knowledge about nutrition in IBD is increasing over time, nutritional suggestions are often underestimated by clinicians. This narrative review is an update summary of current knowledge on nutritional suggestions in IBD, in order to address the impact of nutrition on pathogenesis, micro- and macro-nutrients deficiencies (especially in the case of sarcopenia and obesity), as well as in hospitalized patients.

• Crohn’s disease
• IBD
• anemia
• macronutrients
• micronutrients
• nutrition
• sarcopenia
• ulcerative colitis

• Clinical Trials as Topic
• Hospitalization
• Humans
• Inflammatory Bowel Diseases/diet therapy
• Inflammatory Bowel Diseases/etiology
• Inflammatory Bowel Diseases/physiopathology
• Inflammatory Bowel Diseases/surgery
• Nutritional Physiological Phenomena
• Nutritional Support
• Outpatients

• Hepatocellular carcinoma (HCC)
• inflammatory indexes
• nomogram
• prognostic value
• sarcopenia
• sarcopenic obesity (SO)

• NLRP3 inflammasome
• immunosenescence
• inflammaging
• sarcopenia

• anemia
• end-stage renal disease
• exercise-training
• muscle mass
• oxidative stress

• adiponectin
• aging
• elderly
• muscle mass
• sarcopenia

• Adiponectin/blood
• Female
• Humans
• Male
• Muscle Strength/physiology
• Risk Factors
• Sarcopenia/blood
• Sarcopenia/epidemiology
• Sarcopenia/etiology

• Rehabilitation nutrition
• aging
• muscle wasting
• respiration
• secondary sarcopenia

• Aging/physiology
• Female
• Frailty
• Humans
• Male
• Muscle Strength/physiology
• Respiratory Muscles/physiopathology
• Sarcopenia/complications
• Sarcopenia/diagnosis
• Sarcopenia/pathology
• Sarcopenia/therapy

• INFLAMMAGING
• MUSCLE ATROPHY
• MUSCLE ENVIRONMENTAL CELLS
• NF-κB
• RHEUMATOID ARTHRITIS
• SARCOPENIA
• TNFα
• TRAF6

Measurement of the psoas muscle area has been applied to estimate lean muscle mass as a surrogate marker of sarcopenia, but there is a paucity of evidence regarding the influence of sarcopenia on clinical outcomes following inflammatory bowel disease surgery. The aim of this study was to evaluate the association between MRI enterography defined sarcopenia and postoperative complications in patients undergoing elective ileocaecal resection for Crohn’s disease. To obtain cross sectional area measurement of the psoas muscle, the freehand area tool was used to trace the margin of each psoas muscle at the level of L4, with the sum recorded as Total Psoas Area (TPA). The total cross sectional muscle area of the abdominal wall was recorded as Skeletal Muscle Area (SMA), while myosteatosis was measured by normalising the psoas muscle intensity with the mean intensity of the cerebrospinal fluid. The primary outcome was the incidence of 30-day postoperative complications in patients in the lowest quartile of TPA and SMA. 31 patients were included and ten patients (32.25%) developed postoperative complications within 30 days of surgery. The cut-off values for the lowest quartile for TPA were 11.93 cm² in men and 9.77 cm² in women, including a total of 8 patients (25.8%) with 5 patients in this group (62.5%) developing postoperative complications and 3 patients (37.5%) Clavien-Dindo class ≥ 3 complications. The cut-off values for the lowest quartile for SMA were 73.49 cm² in men and 65.85 cm² in women, with 4 patients out of 8 (50%) developing postoperative complications. Psoas muscle cross sectional area and skeletal mass area can be estimated on Magnetic Resonance Enterography as surrogate markers of sarcopenia with high inter-observer agreement.

• Colorectal surgery
• Crohn’s disease
• Inflammatory bowel disease
• Magnetic resonance imaging
• Psoas muscle
• Sarcopenia

• SIRS
• ascites
• bacterial translocation
• cirrhosis
• hypermetabolism
• sarcopenia

• Adolescent
• Adult
• Aged
• Ascites/microbiology
• Bacterial Translocation
• Body Composition
• Energy Intake
• Energy Metabolism
• Female
• Humans
• Incidence
• Liver Cirrhosis/epidemiology
• Liver Cirrhosis/microbiology
• Liver Cirrhosis/mortality
• Male
• Middle Aged
• Nutritional Status
• Ontario/epidemiology
• Pilot Projects
• Prognosis
• Prospective Studies
• Risk Factors
• Sarcopenia/epidemiology
• Sarcopenia/microbiology
• Sarcopenia/mortality
• Sarcopenia/physiopathology
• Systemic Inflammatory Response Syndrome/epidemiology
• Systemic Inflammatory Response Syndrome/microbiology
• Systemic Inflammatory Response Syndrome/mortality
• Young Adult

Despite the potential detrimental effects of systemic inflammation on muscle mass, which is mainly observed in patients with pathologic diseases, its role in muscle strength, especially in a healthy general population reflecting subclinical low-grade inflammation, is unclear. This is a nationally representative population-based, cross-sectional study from the Korea National Health and Nutrition Examination Survey, which enrolled 1,036 men aged ≥50 years and 1,080 postmenopausal women. After adjustment for confounders, serum high-sensitivity C-reactive protein (hsCRP) level was inversely associated with hand grip strength (HGS) in men. Consistently, compared with men in the lowest serum hsCRP quartile, those in the highest quartile showed a significant lower HGS, with a linear decrease of HGS across increasing serum hsCRP quartiles. Men with low muscle strength had 74.2% higher serum hsCRP than those without, and each standard deviation increment in serum hsCRP was associated with a multivariate-adjusted odds ratio of 1.35 for the risk of low muscle strength in men. However, these associations were not statistically significant in women. These findings provide clinical evidence that chronic subclinical low-grade inflammation may contribute to the deterioration of muscle strength seen with aging, especially in men.

• hand grip strength
• high sensitivity C-reactive protein
• inflammation
• muscle strength
• sarcopenia

Mitochondria orchestrate the life and death of most eukaryotic cells by virtue of their ability to supply adenosine triphosphate from aerobic respiration for growth, development, and maintenance of the ‘physiologic reserve’. Although their double-membrane structure and primary role as ‘powerhouses of the cell’ have essentially remained the same for ~2 billion years, they have evolved to regulate other cell functions that contribute to the aging process, such as reactive oxygen species generation, inflammation, senescence, and apoptosis. Biological aging is characterized by buildup of intracellular debris (e.g., oxidative damage, protein aggregates, and lipofuscin), which fuels a ‘vicious cycle’ of cell/DNA danger response activation (CDR and DDR, respectively), chronic inflammation (‘inflammaging’), and progressive cell deterioration. Therapeutic options that coordinately mitigate age-related declines in mitochondria and organelles involved in quality control, repair, and recycling are therefore highly desirable. Rejuvenation by exercise is a non-pharmacological approach that targets all the major hallmarks of aging and extends both health- and lifespan in modern humans.

• ROS
• aerobic
• aging
• autophagy
• exercise
• inflammation
• lysosome
• mitochondria
• mitophagy
• senescence

Sarcopenia is age‐related muscle wasting that lacks effective therapeutic interventions. We found that systemic ablation of tumor necrosis factor‐α (TNF‐α) prevented sarcopenia and prevented age‐related change in muscle fiber phenotype. Furthermore, TNF‐α ablation reduced the number of satellite cells in aging muscle and promoted muscle cell fusion in vivo and in vitro. Because CD68+ macrophages are important sources of TNF‐α and the number of CD68+ macrophages increases in aging muscle, we tested whether macrophage‐derived TNF‐α affects myogenesis. Media conditioned by TNF‐α‐null macrophages increased muscle cell fusion in vitro, compared to media conditioned by wild‐type macrophages. In addition, transplantation of bone marrow cells from wild‐type mice into TNF‐α‐null recipients increased satellite cell numbers and reduced numbers of centrally nucleated myofibers, indicating that myeloid cell‐secreted TNF‐α reduces muscle cell fusion. Transplanting bone marrow cells from wild‐type mice into TNF‐α‐null recipients also increased sarcopenia, although transplantation did not restore the age‐related change in muscle fiber phenotype. Collectively, we show that myeloid cell‐derived TNF‐α contributes to muscle aging by affecting sarcopenia and muscle cell fusion with aging muscle fibers. Our findings also show that TNF‐α that is intrinsic to muscle and TNF‐α secreted by immune cells work together to influence muscle aging.

• aging
• macrophage
• sarcopenia
• skeletal muscle
• tumor necrosis factor-α

• Adult
• Aged
• Aged, 80 and over
• Aging
• Animals
• Cardiovascular Diseases
• Chronic Disease
• Frail Elderly
• Frailty
• Humans
• Inflammation
• Mice
• Middle Aged

• Z99 AG999999 Intramural NIH HHS

• bone marrow transplantation
• macrophage
• muscle fibrosis
• satellite cell
• skeletal muscle

• nutrition
• rehabilitation
• sarcopenia
• stroke
• systemic inflammation

• Adipokine
• Inflammation
• Interleukin
• Muscle
• Sarcopenia
• Strength

• Aged
• Aged, 80 and over
• Biomarkers/metabolism
• Body Composition/physiology
• Female
• Hand Strength/physiology
• Humans
• Inflammation/metabolism
• Male
• Middle Aged
• Muscle Strength/physiology
• Muscle, Skeletal/metabolism
• Muscle, Skeletal/physiopathology
• Sarcopenia/physiopathology

• 19583 Arthritis Research UK
• MC_U147585827 Medical Research Council
• MC_UU_12011/2 Medical Research Council
• MC_U147585819 Medical Research Council
• MRC_MC_UP_A620_1015 Medical Research Council
• MR/P021220/1 Medical Research Council
• MC_UP_A620_1014 Medical Research Council
• MR/K00414X/1 Medical Research Council
• 19583 Versus Arthritis
• MC_UU_12011/1 Medical Research Council
• G0400491 Medical Research Council
• MC_U147585824 Medical Research Council
• MRC_MC_UU_12011/2 Medical Research Council
• MC_UP_A620_1015 Medical Research Council
• University of Southampton

Elderly and patients affected by chronic diseases face a high risk of muscle loss and impaired physical function. Omega 3 fatty acids (FA) attenuate inflammation and age-associated muscle loss, prevent systemic insulin resistance and improve plasma lipids, potentially impacting on sarcopenia. This paper aims to review recent randomized clinical studies assessing the effects a chronic omega 3 FA supplementation on inflammatory and metabolic profile during conditions characterized by sarcopenia (aging, insulin resistance, type 2 diabetes, chronic renal failure). A comprehensive search of three online databases was performed to identify eligible trials published between 2012 and 2017. A total of 36 studies met inclusion criteria. Omega 3 FA yielded mixed results on plasma triglycerides in the elderly and no effects in renal patients. No changes in systemic insulin resistance were observed. Inflammation markers did not benefit from omega 3 FA in insulin resistant and in renal subjects while decreasing in obese and elderly. Muscle related parameters improved in elderly and in renal patients. In conclusion, in aging- and in chronic disease-associated sarcopenia omega 3 FA are promising independently of associated anabolic stimuli or of anti-inflammatory effects. The evidence for improved glucose metabolism in insulin resistant and in chronic inflammatory states is less solid.

• aging
• chronic kidney disease
• inflammation
• insulin resistance
• omega 3 fatty acids
• sarcopenia

• Dietary inflammatory index
• Inflammation
• Knee osteoarthritis

• Cohort Studies
• Databases, Factual
• Diet/adverse effects
• Diet/methods
• Female
• Humans
• Inflammation/complications
• Inflammation/physiopathology
• Male
• Middle Aged
• Osteoarthritis, Knee/complications
• Osteoarthritis, Knee/diagnostic imaging
• Osteoarthritis, Knee/physiopathology
• Prevalence
• Radiography
• Risk Factors
• Surveys and Questionnaires

• MC_U147585827 Medical Research Council
• MC_U147585819 Medical Research Council
• MC_UP_A620_1014 Medical Research Council
• N01 AR022261 NIAMS NIH HHS
• ICA-CL-2017-03-001 Department of Health
• N01 AR022259 NIAMS NIH HHS
• MC_UU_12011/1 Medical Research Council
• N01 AR022258 NIAMS NIH HHS
• R44 DK103377 NIDDK NIH HHS
• G0400491 Medical Research Council
• N01 AR022262 NIAMS NIH HHS
• N01 AR022260 NIAMS NIH HHS
• MC_U147585824 Medical Research Council

• ANGPTL2
• aging
• catalase
• exercise
• inflammation
• muscle atrophy
• reactive oxygen species (ROS)
• sarcopenia
• satellite cell
• senescence

Ageing is accompanied by chronic inflammatory responses due to elevated circulatory inflammatory cytokine production. Several inflammatory cytokines have been shown to be responsible for a decrease in muscle mass. However, little is known about the possible relationship between inflammation and sarcopaenia. This review aims to summarise the existing evidence about inflammation and sarcopaenia. Sarcopaenia is defined as an age-related decrease of muscle mass and/or muscle strength; it is caused by multiple factors, such as skeletal muscle atrophy, neuromuscular junction degeneration, hormone imbalance, cytokine imbalance, protein synthesis and proteolysis. Several inflammatory cytokines have been considered to promote muscle loss; C-reactive protein levels are significantly upregulated in sarcopaenia and sarcopenic obesity, and high levels of interleukin-6 are associated with reduced muscle mass and muscle strength (the administration of interleukin-6 could lead to a reduction in muscle mass). Up-regulation of tumour necrosis factor-α expression is also related to the development of sarcopaenia. Signalling pathways, such as protein kinase B/mammalian target of rapamycin, Janus kinase/signal transducer and activator of transcription-5 and signal transducer and activator of transcription 3 signalling, involved in muscle metabolism are regulated by insulin-like growth factor-1, tumour necrosis factor-α and interleukin-6 respectively. In conclusion, the inflammatory cytokines produced during chronic inflammation due to ageing, may influence their respective related pathways, thus leading to age-related muscle deterioration.

This review can provide more information for sarcopaenia medicine research in terms of anti-inflammation therapy.

• ageing
• inflammation
• muscle deterioration
• sarcopaenia

• Ageing
• Cytokines
• Inflammaging
• Multi-block partial least squares - discriminant analysis
• Muscle strength
• Short Physical Performance Battery (SPPB)

• Adipose Tissue/diagnostic imaging
• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Aging/blood
• Aging/physiology
• Body Composition
• Cytokines/blood
• Female
• Humans
• Independent Living
• Inflammation/blood
• Inflammation/diagnostic imaging
• Inflammation/physiopathology
• Least-Squares Analysis
• Magnetic Resonance Imaging
• Male
• Muscle Strength
• Muscle, Skeletal/diagnostic imaging
• Muscle, Skeletal/physiology
• Thigh/diagnostic imaging
• Young Adult

• P30 AG028740 NIA NIH HHS