Journal of Cachexia, Sarcopenia and Muscle最新文献_第2页

Annexin A2 Causes Motor Incoordination via Muscle-Cerebellum Axis in Sarcopenia. 肌少症患者膜联蛋白A2通过肌肉-小脑轴引起运动不协调。

IF 9.1 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70203

Xin Jiao, Zengguang Wang, Hanwen Chang, Yongjin Li, Binbin Wang, Xinfa Shao, Yuxin Zhang, Yixuan Lin, Xinlin Jia, Xianhao Zhou, Wentao Li, Dinghao Luo, Tanjun Deng, Xingzuan Lin, Chen Xu, Yaokai Gan, Dongyun Gu

Background: Sarcopenia is a prevalent age-related disorder characterized by progressive muscle atrophy. Impaired balance is one of its most critical clinical consequences, often leading to falling and even bone fractures. As the cerebellum plays a central role in regulating motor coordination, elucidating the molecular mechanisms underlying imbalance in sarcopenia, particularly those mediated by the muscle-cerebellum axis, remains an important yet unresolved question.Methods: 4D label-free proteomics was employed to identify the key secretory protein mediating the interaction between muscles and cerebellums in young and aged mice. Annexin A2 (ANXA2), the candidate protein, was subsequently overexpressed using adeno-associated virus (AAV), and its effects on both muscle and cerebellum were systematically examined. RNA-sequencing was conducted to elucidate the molecular mechanisms underlying ANXA2 function in muscle, while stereotactic injection was performed to investigate its impact on cerebellum and related mechanisms. Finally, we evaluated the therapeutic potential of isoliquiritigenin, an inhibitor of ANXA2, in improving motor coordination and muscle function in aged mice.Results: Aged mice showed obviously impaired motor coordination in the accelerated rotarod (AR) test (p < 0.01) and reduced strength performance in the grip strength assay (p < 0.05) compared to young mice. Proteomic analysis identified ANXA2 as a secretory protein predominantly produced by aged skeletal muscles (p < 0.05 in tibialis anterior, gastrocnemius muscle and quadriceps femoris) but not by other aged organs such as heart, liver, kidney, spleen and lung (all p > 0.05). Functionally, ANXA2 exacerbated muscle atrophy by upregulating atrophy-related markers MuRF-1 and Atrogin-1 (both p < 0.05) and reducing the myotube diameter via regulation of Neuraminidase 2 (Neu2) (p < 0.05). Moreover, ANXA2 was transported into the cerebellum through the blood stream and targeted type 2 cannabinoid receptors (CB2R) in cerebellar Purkinje cells (PCs) of lobule IV/V, thereby contributing to motor incoordination as evidenced by impaired performance in AR tests (p < 0.05). Importantly, isoliquiritigenin, an extract from licorice, effectively inhibited ANXA2 expression in muscle (p < 0.05), alleviated muscle atrophy (p < 0.05) and motor incoordination (p < 0.05), while showing no adverse effects on anxiety-like behaviours associated with CB2R (p > 0.05).Conclusions: ANXA2 is a key mediator of the muscle-cerebellum axis in sarcopenia, contributing to muscle atrophy by downregulating Neu2 and motor incoordination by targeting CB2R. Isoliquiritigenin was identified as an effective compound targeting ANXA2 to improve motor deficits. These findings highlight ANXA2 as a potential therapeutic target and suggest isoliquiritigenin as a promising strategy for alleviating motor incoordination associated with

背景：肌肉减少症是一种以进行性肌肉萎缩为特征的普遍的年龄相关疾病。平衡受损是其最严重的临床后果之一，经常导致跌倒甚至骨折。由于小脑在调节运动协调中起着核心作用，阐明肌肉减少症失衡的分子机制，特别是由肌肉-小脑轴介导的分子机制，仍然是一个重要但尚未解决的问题。方法：采用4D无标记蛋白质组学方法，鉴定幼龄和老年小鼠肌肉与小脑相互作用的关键分泌蛋白。随后使用腺相关病毒（AAV）过表达候选蛋白Annexin A2 (ANXA2)，并系统地检测其对肌肉和小脑的影响。通过rna测序来阐明ANXA2在肌肉中功能的分子机制，通过立体定向注射来研究其对小脑的影响及其相关机制。最后，我们评估了异尿素（一种ANXA2抑制剂）在改善老年小鼠运动协调和肌肉功能方面的治疗潜力。结果：老年小鼠在加速旋转轮（AR）试验中表现出明显的运动协调障碍（p < 0.05）。功能上，ANXA2通过上调萎缩相关标志物MuRF-1和atroggin -1加重肌肉萎缩（p均0.05）。结论：ANXA2是肌少症中肌-小脑轴的关键介质，通过下调Neu2和靶向CB2R导致肌肉萎缩和运动不协调。isoliquirigenin被认为是一种针对ANXA2改善运动缺陷的有效化合物。这些发现强调了ANXA2作为潜在的治疗靶点，并提示异尿酸原素是缓解肌肉减少症相关的运动不协调的有希望的策略。

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引用次数: 0

Effects of Peanut Butter Supplementation on Older Adults' Physical Function: A 6-Month Randomised Controlled Trial. 补充花生酱对老年人身体功能的影响：一项为期6个月的随机对照试验。

IF 9.1 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70221

Ilili Feyesa, Jeew Hettiarachchi, Robin M Daly, Elena S George, Ekavi N Georgousopoulou, David Scott, Brenton J Baguley, Gavin Abbott, Sze-Yen Tan

Background: Nut consumption has been associated with a reduced risk of functional decline, but evidence from randomised controlled trials to support functional benefit is lacking. Therefore, this study aimed to investigate whether daily supplementation of peanut butter over 6 months, relative to usual care, can improve physical function in community-dwelling older adults.

Methods: One hundred and twenty older adults (aged ≥ 65 years) at risk of falls were randomly assigned to receive peanut butter (43 g/day, n = 60) or maintain usual care (control, n = 60) for 6 months. Outcomes assessed at baseline and 6 months included physical function (4-m gait speed [primary outcome], standing balance test, four-square step test [FSST], five times sit-to-stand [5STS] test time and muscle power, 30-s sit-to-stand (30-s STS) and timed up and go [TUG] tests), muscle strength (handgrip [HGS] and isometric knee extensor strength tests [KES]) and anthropometry/body composition (weight, body mass index [BMI], total lean and fat mass and appendicular lean mass). Linear regression models, adjusting for age, sex, baseline value of the dependent variable, BMI, physical activity and diet quality, estimated intention-to-treat intervention effects.

Results: A total of 108 (90%) participants completed the study. At baseline, 70% were female, and the mean ± SD age and BMI were 76.1 ± 4.6 years and 27.5 ± 4.2 kg/m², respectively. At 6 months, there were no significant treatment effects on the primary outcome of gait speed or other measures of physical function (p > 0.05), with the exception that 5STS time and muscle power improved significantly more in the peanut butter compared to control group (estimated treatment effect: time, -1.23 s [95% CI, -2.09, -0.37], p = 0.006; absolute power, 22.0 W [95% CI: 7.1 to 36.9], p = 0.004; relative power, 0.27 W/kg [95% CI: 0.10 to 0.45], p = 0.002). Changes in HGS, KES, weight, BMI, total fat mass, total lean mass or appendicular lean mass did not differ between groups. In the peanut butter group, among those who completed the follow-up, the mean (SD) adherence was 86.0 (13.8) %.

Conclusion: In community-dwelling older adults at risk for falls, daily peanut butter consumption for 6 months improved 5STS time and muscle power based on 5STS, but not gait speed, muscle strength or body composition.

Trial registration: Australian New Zealand Clinical Trials: ACTRN12622001291774.

背景：坚果食用与功能衰退风险降低有关，但缺乏随机对照试验支持功能益处的证据。因此，本研究旨在调查在6个月的时间里，相对于常规护理，每天补充花生酱是否可以改善社区居住老年人的身体功能。方法：120名有跌倒风险的老年人（年龄≥65岁）被随机分配到接受花生酱（43 g/天，n = 60）或维持常规护理（n = 60） 6个月。基线和6个月时评估的结果包括身体功能（4米步态速度[主要结果]、站立平衡测试、四平方步测试[FSST]、5次坐立[5STS]测试时间和肌肉力量、30秒坐立（30秒STS）和计时起跑[TUG]测试）、肌肉力量（握力[HGS]和等距膝关节伸肌力量测试[KES]）和人体测量/身体组成（体重、体重指数[BMI]、总瘦、总脂肪质量和尾侧瘦质量）。线性回归模型，调整了年龄、性别、因变量基线值、BMI、身体活动和饮食质量，估计了意向治疗干预效果。结果：共有108名（90%）参与者完成了研究。基线时，70%为女性，平均±SD年龄和BMI分别为76.1±4.6岁和27.5±4.2 kg/m2。在6个月时,治疗没有明显影响步态速度或其他措施的主要结果的物理作用(p > 0.05),除了5 sts时间和肌肉力量明显改善更多的花生酱相比对照组(估计治疗效果:时间,-1.23(95%可信区间,-2.09,-0.37),p = 0.006;绝对权力,22.0 W(95%置信区间CI: 7.1 - 36.9), p = 0.004;相对功率0.27 W / kg(95%置信区间CI: 0.10 - 0.45), p = 0.002)。各组间HGS、KES、体重、BMI、总脂肪质量、总瘦质量或阑尾瘦质量的变化无差异。在花生酱组中，在完成随访的患者中，平均（SD）依从性为86.0(13.8)%。结论：在有跌倒风险的社区老年人中，每天食用花生酱6个月可以改善5STS时间和基于5STS的肌肉力量，但不能改善步态速度、肌肉力量或身体成分。试验注册：澳大利亚新西兰临床试验：ACTRN12622001291774。

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引用次数: 0

Prediabetes Associates With Musculoskeletal Alterations Independent of Total Body Adiposity. 前驱糖尿病与独立于全身肥胖的肌肉骨骼改变相关。

IF 8.9 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70198

Alan Fappi,Clifton J Holmes,Chao Cao,Vasavi Shabrish,Aman P Aher,Karen Shen,Paul K Commean,Dwight A Towler,Dominic N Reeds,Gretchen A Meyer,Bettina Mittendorfer

BACKGROUNDExcess adiposity is a major risk factor for insulin resistance, prediabetes, and Type 2 diabetes and increases the risk for sarcopenia and osteosarcopenia later in life. It has been proposed that altered metabolic function and musculoskeletal status in people with obesity are directly linked, presumably because they share common pathophysiological mechanisms. However, the effect of metabolic dysfunction, independent of adiposity, on musculoskeletal status is unknown.METHODSWe performed a comprehensive assessment of musculoskeletal status in people with overweight/obesity and prediabetes (n = 12; 72% women; age: 67 ± 6 years; weight: 81 ± 11 kg; mean ± SD) and a control group of sex-, age- and adiposity-matched participants with normoglycaemia (n = 18; 67% women; age: 65 ± 6 years; weight: 81 ± 12 kg).RESULTSAppendicular muscle mass expressed relative to the sarcopenia threshold (-5.6% ± 2.5% vs. 1.8% ± 2.0%; mean ± SEM) and the bone mineral density T-score (-0.22 ± 0.41 vs. 0.82 ± 0.33) were lower (p < 0.05) in the prediabetic group than the control group. Additionally, the prediabetic group had ~25% smaller (by cross-sectional area) myofibres and ~40% fewer muscle Type 2 macrophages (all p < 0.05), whereas intramyocellular lipid content was more than 50% higher (p < 0.05) in the prediabetic than the control group. Maximal muscle strength was not different between the two groups, but muscle strength during repeated maximum voluntary contractions declined more (p < 0.05) in the prediabetic group.CONCLUSIONIn people with overweight/obesity, metabolic dysfunction associates with musculoskeletal dysfunction independent of adiposity.

背景：过度肥胖是胰岛素抵抗、前驱糖尿病和2型糖尿病的主要危险因素，并增加晚年肌肉减少症和骨骼肌减少症的风险。有人提出，肥胖人群的代谢功能和肌肉骨骼状态的改变是直接相关的，可能是因为它们具有共同的病理生理机制。然而，独立于肥胖的代谢功能障碍对肌肉骨骼状态的影响尚不清楚。方法：我们对超重/肥胖和前驱糖尿病患者（n = 12, 72%女性，年龄：67±6岁，体重：81±11 kg，平均±SD）和对照组（n = 18, 67%女性，年龄：65±6岁，体重：81±12 kg）的肌肉骨骼状况进行了全面评估。结果糖尿病前期组相对于肌少症阈值的阑尾肌质量表达（-5.6%±2.5%比1.8%±2.0%；平均值±SEM）和骨密度t评分（-0.22±0.41比0.82±0.33）均低于对照组（p < 0.05）。此外，糖尿病前期组肌纤维（按横截面积计算）减少约25%，肌肉2型巨噬细胞减少约40%（均p < 0.05），而糖尿病前期组的细胞内脂质含量比对照组高50%以上（p < 0.05）。两组最大肌力差异无统计学意义，但糖尿病前期组反复最大自主收缩时肌力下降幅度更大（p < 0.05）。结论：在超重/肥胖人群中，代谢功能障碍与肌肉骨骼功能障碍相关，独立于肥胖。

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引用次数: 0

EIF4A3-Induced Circular RNA circSnd1 Promotes Muscle Atrophy and Muscle Ageing by Stabilizing EEF1A1. eif4a3诱导的环状RNA circSnd1通过稳定eif1a1促进肌肉萎缩和肌肉老化。

IF 8.9 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70210

Jin Li,Bing Jin,Yuwei Yan,Yuying Chen,Xiaohang Yin,Xinyi Ren,Qian Li,Jingying Chen,Siqi Wang,Tingting Yang,Yanan Zhang,Qiumeng Nie,Dongchao Lu,Ming Wu,Yan Yu,Lei Chen,Tarun Keswani,Guoping Li,Dragos Cretoiu,T Scott Bowen,Junjie Xiao,Yongjun Zheng

BACKGROUNDMuscle atrophy is a common complication of ageing, and many chronic conditions, lacks defined therapeutic interventions. It is still mostly unknown how circular RNAs contribute to muscle atrophy.METHODScircRNA sequencing and quantitative real-time PCR were performed to detect the changed circRNAs in muscle atrophy models and aged muscle. Then the gain-of-function and loss-of-function experiments were used to investigate the function of circSnd1 in muscle atrophy and muscle ageing. Furthermore, we used RIP-MS and RIP assay to determine the downstream and upstream mechanism of circSnd1 in muscle atrophy.RESULTSHere, we characterized the function and mechanism of highly species-conserved circRNA derived from staphylococcal nuclease and Tudor domain containing 1 gene (named circSnd1) in muscle atrophy. CircSnd1 is upregulated in many types of muscle atrophy models in both in vivo and in vitro (all p < 0.01). Meanwhile, circSnd1 is also higher expressed in aged muscle in humans (+2.2-fold, n = 5, p < 0.05), mice (+43.96%, n = 6, p < 0.05) and myotubes (+42.21%, n = 6, p < 0.05). Functional analyses show that circSnd1 promotes muscle atrophy and muscle ageing at the cellular level and mouse level while repressing it ameliorates multiple types of muscle atrophy (all p < 0.05). Mechanistically, the RNA binding protein eukaryotic translation initiation factor 4A3 (EIF4A3) can bind to the intron flanking sequence of circSnd1 to induce circSnd1 cyclization and increase circSnd1 expression in muscle atrophy. In addition, circSnd1 promotes the binding between human HLA-F adjacent transcript 10 (FAT10) and eukaryotic translation elongation factor 1 alpha 1 (EEF1A1). FAT10 competes with ubiquitin for binding with EEF1A1, which decreases the ubiquitination of EEF1A1 and stabilizes the protein level of EEF1A1 in muscle cells to promote atrophy.CONCLUSIONSWe have identified circSnd1 as a novel circRNA that promotes muscle atrophy and highlighted its potential as a novel therapeutic target.

肌肉萎缩是衰老和许多慢性疾病的常见并发症，缺乏明确的治疗干预措施。环状rna是如何导致肌肉萎缩的，目前还不得而知。方法采用scircrna测序和实时荧光定量PCR检测肌肉萎缩模型和衰老肌肉中circrna的变化。然后通过功能获得和功能丧失实验研究circSnd1在肌肉萎缩和肌肉老化中的功能。此外，我们还利用RIP- ms和RIP实验确定了circSnd1在肌肉萎缩中的上下游机制。结果本研究鉴定了葡萄球菌核酸酶和Tudor结构域1基因（circSnd1）衍生的高度物种保守的circRNA在肌肉萎缩中的功能和机制。CircSnd1在体内和体外多种肌肉萎缩模型中表达上调（均p < 0.01）。同时，circSnd1在人类衰老肌肉（+2.2倍，n = 5, p < 0.05）、小鼠（+43.96%,n = 6, p < 0.05）和肌管（+42.21%,n = 6, p < 0.05）中的表达量也较高。功能分析表明，circSnd1在细胞水平和小鼠水平上促进肌肉萎缩和肌肉老化，抑制其可改善多种类型的肌肉萎缩（p < 0.05）。在机制上，RNA结合蛋白真核翻译起始因子4A3 （EIF4A3）可以结合circSnd1的内含子侧翼序列，诱导circSnd1环化，增加肌肉萎缩中circSnd1的表达。此外，circSnd1促进人HLA-F相邻转录本10 （FAT10）与真核翻译延伸因子1 α 1 （EEF1A1）的结合。FAT10与泛素竞争与EEF1A1结合，降低EEF1A1的泛素化，稳定肌肉细胞中EEF1A1的蛋白水平，促进萎缩。结论：我们已经确定circSnd1是一种促进肌肉萎缩的新型环状rna，并强调了其作为一种新的治疗靶点的潜力。

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引用次数: 0

RETRACTION: Nestin Regulates Autophagy-Dependent Ferroptosis Mediated Skeletal Muscle Atrophy by Ubiquitinating MAP 1LC3B. 回顾：巢蛋白通过泛素化MAP 1LC3B调控自噬依赖性铁下垂介导的骨骼肌萎缩。

IF 9.1 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70235

引用次数: 0

Temporal Dynamics and Bidirectional Longitudinal Association Between Physical Function and Depressive Symptoms in Older Adults. 老年人身体功能与抑郁症状的时间动态和双向纵向关联

IF 8.9 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70223

Belayneh Mengist,Mojtaba Lotfaliany,Julie A Pasco,Bruno Agustini,Michael Berk,Suzanne G Orchard,Joanne Ryan,Alice J Owen,Robyn L Woods,John J McNeil,Mohammadreza Mohebbi

BACKGROUNDPhysical function decline and depression are major challenges of the rapidly growing older population. This longitudinal study aimed to investigate the bidirectional longitudinal association between physical function and depressive symptoms, which are poorly understood in older adults.METHODSWe utilised data from the ASPirin in Reducing Events in the Elderly (ASPREE) clinical trial and extended follow-up cohort between 2010 and 2022. The presence of depressive symptoms was defined as a score of ≥ 8 on the Center for Epidemiologic Studies Depression 10-item scale. Physical function was assessed using gait speed for physical performance and handgrip strength for muscle strength. Gait speed and handgrip strength were categorised using the European Working Group on Sarcopenia in Older People (EWGSOP2) cut-off points. The bidirectional association between physical function and depressive symptoms was estimated using generalised estimating equations models. The robustness of the longitudinal bidirectional relationship was assessed using random-intercept cross-lagged panel models.RESULTSAmong 19 114 ASPREE participants, 15 854 (56% females) older adults (mean age 75 years) were included in the analysis. During a median follow-up of 8.4 years, participants with combined poor physical performance and weak muscle strength had 81% higher odds of developing depressive symptoms compared to those with good performance and strength (OR = 1.81, 95% CI: 1.55-2.11). Conversely, participants with depressive symptoms had 70% higher odds of reduced physical function (combined poor physical performance and weak muscle strength) compared to those with no depressive symptoms (OR = 1.70, 95% CI: 1.61-1.80). The random-intercept cross-lagged panel models verified the bidirectional longitudinal associations between physical function and depressive symptoms across the follow-up waves.CONCLUSIONSReduced physical function and depressive symptoms are associated bidirectionally over time of a similar magnitude. Understanding this reciprocal association is crucial for developing effective prevention and treatment strategies for physical and mental health conditions.

身体机能下降和抑郁是快速增长的老年人口面临的主要挑战。这项纵向研究旨在调查身体功能和抑郁症状之间的双向纵向关联，这在老年人中知之甚少。方法：我们使用了2010年至2022年阿司匹林减少老年人事件（ASPREE）临床试验和扩展随访队列的数据。在流行病学研究中心抑郁10项量表中，出现抑郁症状的定义为得分≥8分。身体功能的评估用步态速度来衡量身体表现，用握力来衡量肌肉力量。采用欧洲老年人肌肉减少症工作组（EWGSOP2）的分界点对步态速度和握力进行分类。使用广义估计方程模型估计身体功能与抑郁症状之间的双向关联。纵向双向关系的稳健性评估使用随机截距交叉滞后面板模型。结果19 114名ASPREE参与者中，15 854名老年人（56%为女性）（平均年龄75岁）被纳入分析。在中位随访8.4年期间，身体表现差和肌肉力量弱的参与者与身体表现和力量好的参与者相比，出现抑郁症状的几率高出81% （OR = 1.81, 95% CI: 1.55-2.11）。相反，与没有抑郁症状的参与者相比，有抑郁症状的参与者身体功能下降（包括身体表现差和肌肉力量弱）的几率高出70% （OR = 1.70, 95% CI: 1.61-1.80）。随机截距交叉滞后面板模型验证了身体功能与抑郁症状之间的双向纵向关联。结论随着时间的推移，身体功能下降和抑郁症状呈双向相关，且程度相似。了解这种相互关联对于制定有效的身心健康状况预防和治疗策略至关重要。

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引用次数: 0

Increased Skeletal Muscle Fat in Patients With Haematological Cancer Is Associated With Reduced Cardiorespiratory Fitness. 血液学癌症患者骨骼肌脂肪增加与心肺功能降低相关

IF 8.9 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70186

Nicholas J Saner,Stephen J Foulkes,Hayley T Dillon,Lauren Burnham,Richard Thompson,Andre La Gerche,Mark J Haykowsky,Erin J Howden

BACKGROUNDPatients with haematological cancer often exhibit reduced cardiorespiratory fitness and an elevated risk of cardiovascular disease. The mechanisms underlying this impairment are multifactorial, but the contribution of skeletal muscle fat infiltration has not been evaluated. This study aimed to compare thigh skeletal muscle fat fraction (SMFF) in patients with haematological cancer to healthy controls and to assess the contribution of SMFF to cardiorespiratory fitness in this cohort.METHODSWe performed a cross-sectional analysis of patients with haematological cancer (n = 70, 61% male, age: 51 ± 16 years) and age- and sex-matched healthy controls (n = 70, 61% male, age: 50 ± 15 years). Thigh SMFF was assessed via magnetic resonance imaging. We also measured cardiorespiratory fitness (peak oxygen uptake, V̇O2peak), global longitudinal strain (GLS) via echocardiography and haemoglobin concentrations in the haematological cancer cohort. Hierarchical multiple regression analysis was performed to identify predictors of V̇O2peak.RESULTSSMFF was higher in the haematological cancer cohort versus the healthy control cohort (11.0% ± 3.4% vs. 8.8% ± 3.8%, p = 0.001). V̇O2peak was significantly lower than predicted values for the haematological cancer cohort (mean difference; 9.61 ± 8.30 mL.kg-1.min-1, p < 0.001). The multiple regression analysis accounted for 35% of the variance in V̇O2peak with both SMFF (β = -0.40, ΔR2 = 0.14, p = 0.002) and haemoglobin concentrations (β = 0.50, ΔR2 = 0.23, p < 0.001) being significant independent predictors of V̇O2peak, while skeletal muscle volume (β = 0.00, ΔR2 = 0.00, p = 0.767), GLS (β = 0.06, ΔR2 = 0.00, p = 0.509), prior anthracycline treatment (β = 0.00, ΔR2 = 0.00, p = 0.962) and clinical diagnosis (β = 0.00, ΔR2 = 0.00, p = 0.555) were not.CONCLUSIONSSMFF is increased in haematological cancer patients and contributes to reduced V̇O2peak. Consequently, increased SMFF may be an important target to improve cardiovascular health and cardiorespiratory fitness in this population.

血液学癌症患者通常表现为心肺功能下降和心血管疾病风险升高。这种损伤的机制是多因素的，但骨骼肌脂肪浸润的作用尚未得到评估。本研究旨在比较血液学癌症患者与健康对照者的大腿骨骼肌脂肪分数（SMFF），并评估SMFF对该队列中心肺健康的贡献。方法我们对血液癌患者（n = 70, 61%男性，年龄51±16岁）和年龄和性别匹配的健康对照（n = 70, 61%男性，年龄50±15岁）进行了横断面分析。通过磁共振成像评估大腿SMFF。在血液学癌症队列中，我们还通过超声心动图测量了心肺适能（峰值摄氧量、V / o峰值）、总体纵向应变（GLS）和血红蛋白浓度。采用分层多元回归分析确定预测指标。结果血液病组smff高于健康对照组（11.0%±3.4%比8.8%±3.8%,p = 0.001）。血液学癌症组的V²o2峰值显著低于预测值（平均差值：9.61±8.30 mL.kg-1）。Min-1, p < 0.001)。多重回归分析占35%的方差在V̇O2peak与SMFF(β= -0.40,ΔR2 = 0.14, p = 0.002)和血红蛋白浓度(β= 0.50,ΔR2 = 0.23, p < 0.001)显著独立预测V̇O2peak,而骨骼肌体积(β= 0.00,ΔR2 = 0.00, p = 0.767), gl(β= 0.06,ΔR2 = 0.00, p = 0.509),之前蒽环霉素治疗(β= 0.00,ΔR2 = 0.00, p = 0.962)和临床诊断(β= 0.00,ΔR2 = 0.00, p = 0.555)。结论ssmff在血液学肿瘤患者中升高，并与降低vo2峰有关。因此，增加SMFF可能是改善该人群心血管健康和心肺健康的重要目标。

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引用次数: 0

Age-Stratified Associations of Sarcopenic Obesity With Mortality in Type 2 Diabetes. 2型糖尿病患者肌肉减少型肥胖与死亡率的年龄分层关系

IF 8.9 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70211

Shinta Yamamoto,Yoshitaka Hashimoto,Fuyuko Takahashi,Moe Murai,Nozomi Yoshioka,Yuto Saijyo,Chihiro Munekawa,Hanako Nakajima,Noriyuki Kitagawa,Takafumi Osaka,Ryosuke Sakai,Hiroshi Okada,Naoko Nakanishi,Saori Majima,Emi Ushigome,Masahide Hamaguchi,Michiaki Fukui

BACKGROUNDSarcopenic obesity, the coexistence of sarcopenia and obesity, has been linked to adverse health outcomes due to comorbidity. Evidence on the association between sarcopenic obesity and mortality among individuals with Type 2 diabetes remains limited METHODS: Sarcopenic obesity was defined using Japan Working Group on Sarcopenic Obesity criteria. Participants were divided into four groups based on the presence of sarcopenia and obesity. Cox proportional hazards models evaluated the mortality risk. Subgroup analyses were performed by age (40-75 vs. >75 years). Sensitivity analysis was performed by dichotomizing participants into sarcopenic obesity and non-sarcopenic obesity groups.RESULTSOf the 799 participants (mean age 68.6 years, 59.3% men), proportions of neither sarcopenia nor obesity, obesity alone, sarcopenia alone and sarcopenic obesity were 56.2%, 34.5%, 6.3% and 3.0%, respectively. During a median follow-up of 46 months, 41 deaths occurred. Compared with neither of them, the adjusted hazard ratios (aHRs) (95% CI) of mortality in obesity alone, sarcopenia alone and sarcopenic obesity were 0.53 (0.18-1.57) (p = 0.25), 2.36 (0.99-5.6) (p = 0.053) and 2.89 (1.01-8.30) (p = 0.048), respectively. Age-stratified analyses revealed that sarcopenic obesity markedly increased mortality risk in participants aged 40-75 years (aHR 13.1 [2.93-58.4], p < 0.001), whereas sarcopenia alone (aHR 3.21 [1.07-8.33], p = 0.004), but not sarcopenic obesity (aHR 1.41 [0.34-8.81], p = 0.51), was associated with increased mortality in those aged > 75 years. Compared with non-sarcopenic obesity, sarcopenic obesity had a significantly higher hazard ratio for mortality (aHR 4.0 [1.44-11.0], p = 0.008). In age-stratified analysis, this association remained significant in participants aged 40-75 years (aHR 14.1 [3.25-61.5], p < 0.001), but not in those aged > 75 years (aHR 1.55 [0.32-7.46], p = 0.59) (interaction p = 0.03).CONCLUSIONSIn Japanese individuals with Type 2 diabetes, sarcopenic obesity was significantly associated with increased mortality risk. This relationship was particularly pronounced in individuals aged 40-75 years, whereas sarcopenia alone was associated with increased mortality risk rather than sarcopenic obesity in individuals aged > 75.

背景：肌肉减少型肥胖，即肌肉减少症和肥胖的共存，由于合并症而与不良的健康结果有关。关于2型糖尿病患者肌肉减少性肥胖与死亡率之间关系的证据仍然有限。方法：使用日本肌肉减少性肥胖工作组的标准来定义肌肉减少性肥胖。参与者根据肌肉减少症和肥胖的情况被分为四组。Cox比例风险模型评估死亡风险。按年龄进行亚组分析（40-75岁vs. 50 -75岁）。通过将参与者分为肌肉减少型肥胖组和非肌肉减少型肥胖组进行敏感性分析。结果在799名参与者中（平均年龄68.6岁，男性59.3%），既没有肌肉减少症也没有肥胖、肥胖、肌肉减少症和肌肉减少性肥胖的比例分别为56.2%、34.5%、6.3%和3.0%。在平均46个月的随访期间，发生了41例死亡。与两者相比，单独肥胖、单独肌肉减少症和肌肉减少性肥胖的校正危险比（ahr）（95% CI）分别为0.53 (0.18-1.57)（p = 0.25）、2.36 (0.99-5.6)（p = 0.053）和2.89 (1.01-8.30)（p = 0.048）。年龄分层分析显示，40-75岁参与者的肌肉减少性肥胖显著增加死亡风险（aHR 13.1 [2.93-58.4], p 75）。与非肌肉减少性肥胖相比，肌肉减少性肥胖的死亡率风险比显著高于非肌肉减少性肥胖（aHR 4.0 [1.44-11.0], p = 0.008）。在年龄分层分析中，这种相关性在40-75岁的参与者中仍然显著(aHR为14.1 [3.25-61.5]，p为75 (aHR为1.55 [0.32-7.46],p = 0.59)（交互作用p = 0.03）。结论：在日本2型糖尿病患者中，肌肉减少型肥胖与死亡风险增加显著相关。这种关系在40-75岁的个体中尤为明显，而在75岁的个体中，肌肉减少症单独与死亡风险增加有关，而不是肌肉减少性肥胖。

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引用次数: 0

Association of Sarcopenia and Lower Bone Density With Positional Vertigo in the Morning: Insights From a Nationwide Survey. 肌肉减少症和低骨密度与早晨体位性眩晕的关系：来自一项全国性调查的见解。

IF 9.1 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-02-01 DOI: 10.1002/jcsm.70219

Eun Ji Kim, Eunjin Kwon, Sukyoung Jung, Ji-Soo Kim, Seong-Hae Jeong

Background: This study aimed to identify associations of sarcopenia, obesity and low bone mineral density (BMD) with morning positional vertigo (PV) and to examine whether these associations differ according to vestibular function status in a nationally representative sample of Korean adults.

Methods: We analysed data from 8512 adults aged ≥ 40 years (50.03% women, mean ± standard error [SE] = 54.06 ± 0.19) who participated in the Korean National Health and Nutrition Examination Survey 2008-2010. Morning PV was defined as severe vertigo when turning in bed or rising in the morning within the past year. Vestibular impairment was assessed using the modified Romberg test (eyes closed, standing on a compliant foam surface). Participants were classified into three groups: controls (no dizziness), morning PV with normal Romberg test results and morning PV with abnormal Romberg test results (suggesting vestibular dysfunction). Body composition-including appendicular skeletal muscle mass, fat mass and BMD-was measured. Sarcopenia was defined according to the Asian Working Group for Sarcopenia 2019 criteria, and abnormal BMD was defined as T-score < 1.0. Weighted multinomial logistic regression analyses were adjusted for age, sex, income, comorbidities, lifestyle and psychosocial variables.

Results: The weighted 1-year prevalence of morning PV was 12.58% (95% confidence interval [CI], 11.38-13.89). Abnormal Romberg performance, indicating vestibular dysfunction, was present in 0.96% of all survey respondents and in 7.66% of those with morning PV. Participants with vestibular-impaired morning PV were older (mean age ± SE = 66.47 ± 1.49), predominantly women, and had higher rates of sarcopenia (38.33%) and low BMD (86.39%) than controls. In adjusted models, sarcopenia independently predicted vestibular-impaired morning PV (odds ratio [OR], 1.94; 95% CI, 1.14-3.29; p = 0.014). Sensitivity analysis restricted to current morning PV confirmed the association between sarcopenia and vestibular impairment (OR, 2.97; 95% CI, 1.08-8.12; p = 0.035) and demonstrated that lower BMD (minimum T-score) was inversely associated with vestibular dysfunction (OR, 0.49; 95% CI, 0.25-0.99; p = 0.046).

Conclusions: Morning PV is common among middle-aged and older adults and is associated with systemic frailty markers, particularly sarcopenia and bone loss, in the presence of vestibular dysfunction. These associations were more pronounced in older adults, suggesting a vestibulo-musculoskeletal interaction that may contribute to balance impairment and functional decline with aging. Screening for sarcopenia and bone health, along with vestibular and lifestyle interventions, may help reduce recurrent vertigo and improve functional aging.

背景：本研究旨在确定肌肉减少症、肥胖和低骨密度（BMD）与早晨体位性眩晕（PV）的关系，并在具有全国代表性的韩国成年人样本中检查这些关系是否根据前庭功能状态而有所不同。方法：我们分析了参加2008-2010年韩国国家健康与营养调查的8512名年龄≥40岁的成年人（50.03%为女性，平均±标准误差[SE] = 54.06±0.19）的资料。早晨PV被定义为过去一年内在床上翻身或早晨起床时出现的严重眩晕。使用改进的Romberg测试（闭上眼睛，站在柔软的泡沫表面上）评估前庭损伤。参与者分为三组：对照组（无头晕）、Romberg试验结果正常的晨间PV和Romberg试验结果异常的晨间PV（提示前庭功能障碍）。测量身体组成，包括阑尾骨骼肌量、脂肪量和骨密度。根据亚洲肌少症工作组2019标准定义肌少症，并将骨密度异常定义为t评分。结果：晨起PV的加权1年患病率为12.58%（95%置信区间[CI]， 11.38-13.89）。0.96%的调查对象和7.66%的晨间PV患者存在Romberg表现异常，表明前庭功能障碍。前庭损伤的晨间PV患者年龄较大（平均年龄±SE = 66.47±1.49），以女性为主，肌肉减少症发生率（38.33%）和低骨密度（86.39%）高于对照组。在调整后的模型中，肌少症独立预测前庭损伤的晨间PV（比值比[OR]， 1.94; 95% CI, 1.14-3.29; p = 0.014）。仅限于当前早晨PV的敏感性分析证实了肌肉减少症与前庭功能障碍之间的关联（OR, 2.97; 95% CI, 1.08-8.12; p = 0.035），并表明较低的骨密度（最小t评分）与前庭功能障碍呈负相关（OR, 0.49; 95% CI, 0.25-0.99; p = 0.046）。结论：晨间PV在中老年人群中很常见，与前庭功能障碍下的系统性衰弱标志物有关，尤其是肌肉减少症和骨质流失。这些关联在老年人中更为明显，表明前庭-肌肉-骨骼的相互作用可能导致平衡障碍和功能衰退。筛查肌肉减少症和骨骼健康，以及前庭和生活方式干预，可能有助于减少复发性眩晕和改善功能性衰老。

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引用次数: 0

Sit-to-Stand Power From 2D Pose Estimation as an Indicator of Muscle Strength in Older Adults 从2D姿势估计的坐姿到站立的力量作为老年人肌肉力量的指标

IF 8.9 1区医学

Journal of Cachexia, Sarcopenia and Muscle

Pub Date : 2026-01-26 DOI: 10.1002/jcsm.70208

Wonjae Hwang, Dain Shim, Joowan Kim, Kyung Rok Oh, Sun Gun Chung, Jaewon Beom, Myung Woo Park, Kyung Su Kim, Joonghee Kim, Chul Hyun Park, Keewon Kim

The sit-to-stand (STS) test is a crucial tool for sarcopenia assessment. However, the two most widely used diagnostic frameworks differ in their conceptualization of the test. The European Working Group on Sarcopenia in Older People 2 views the STS test primarily as a proxy for muscle strength, while the Asian Working Group for Sarcopenia 2019 (AWGS 2019) classifies it as a measure of physical performance. This discrepancy poses challenges to conceptual clarity in both research and practice. Recent advancements in pose-estimation algorithms allow for kinematic assessment using a standard handheld devices, providing a simple and cost-effective alternative to conventional motion-analysis.

坐立（STS）测试是评估肌肉减少症的重要工具。然而，两种最广泛使用的诊断框架在测试的概念上有所不同。欧洲老年人肌肉减少症工作组2将STS测试主要视为肌肉力量的代表，而亚洲肌肉减少症工作组2019 （AWGS 2019）将其归类为身体表现的衡量标准。这种差异对研究和实践中的概念清晰度提出了挑战。姿态估计算法的最新进展允许使用标准手持设备进行运动学评估，为传统的运动分析提供了一种简单且具有成本效益的替代方案。

引用次数: 0