Hongrui Chen, Zening Huang, Qinqi Yu, Bin Sun, Chen Hua, Xiaoxi Lin
{"title":"Comment on 'Effects of Sarcopenia and Frailty on Postoperative Recovery in Elderly Patients: A Prospective Cohort Study' by Guo et al.","authors":"Hongrui Chen, Zening Huang, Qinqi Yu, Bin Sun, Chen Hua, Xiaoxi Lin","doi":"10.1002/jcsm.13625","DOIUrl":"https://doi.org/10.1002/jcsm.13625","url":null,"abstract":"","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aikaterini Kamiliou, Vasileios Lekakis, George Xynos, Evangelos Cholongitas
We read with great interest the article by Lu et al. [1] regarding the impact of myosteatosis on post–liver transplantation (LT) outcome in males transplanted for hepatocellular carcinoma (HCC). The authors reported a relatively low prevalence of myosteatosis (27.8% in males) using a gender-based definition (i.e., muscle attenuation less than 37.5 HU at the third lumbar vertebra of cross-sectional CT image for men). However, in our recently published meta-analysis [2] including 10 studies with 3316 HCC patients, the overall pooled prevalence of myosteatosis was estimated as high as 50% (95% confidence interval [CI] 35%–65%) [2]. This discrepancy could be attributed to the fact that Lu et al. [1] included mainly chronic hepatitis B–associated HCC patients, although all patients were Asians. Indeed, our meta-analysis showed that the prevalence of myosteatosis is significantly lower in Asian HCC patients, compared to the non-Asian HCC patients (pooled prevalence 45% vs. 69%, respectively, p = 0.02), whereas viral-associated HCC patients have significantly less frequently myosteatosis, compared to those with fatty or alcoholic liver disease–associated HCC (pooled prevalence 49% vs. 65% vs. 86%, respectively, p < 0.001). Interestingly, the authors [1] concluded that myosteatosis was not associated with post-LT outcome in females, although they did not provide which cutoff was used for definition of myosteatosis in this subgroup, although no clear explanation was given for this finding. In addition, they found no association between myosteatosis and hepatic encephalopathy although our meta-analysis [3] showed that cirrhotic patients with myosteatosis, compared to those without myosteatosis, have more frequently a previous history of hepatic encephalopathy (32% vs. 15%, p = 0.04) possibly related with the reduction of skeletal muscle capacity to remove ammonia. Finally, it would be interesting if the authors evaluated the impact of diabetes mellitus, which is an known factor associated with myosteatosis and poor prognosis after LT [3, 4], as well as if they compared the post-LT outcome of HCC patients with sarcopenia and myosteatosis/isolated myosteatosis versus those with isolated sarcopenia, as recent studies have shown that myosteatosis may be a more important factor, compared to sarcopenia, in the pre-LT setting of patients without HCC [5].
Nevertheless, Lu et al. [1] confirmed the predictive role of myosteatosis in HCC patients not only in the pre-LT setting [2] but also in the post-LT outcome [1], indicating the importance of including assessment of myosteatosis in the process for LT evaluation. However, their results [1] need validation in non-Asian populations, in which the aetiology of liver disease is more frequently metabolic and alcohol-related HCC.
{"title":"Comment on ‘Myosteatosis and Muscle Loss Impact Liver Transplant Outcomes in Male Patients With Hepatocellular Carcinoma’ by Lu et al.","authors":"Aikaterini Kamiliou, Vasileios Lekakis, George Xynos, Evangelos Cholongitas","doi":"10.1002/jcsm.13620","DOIUrl":"https://doi.org/10.1002/jcsm.13620","url":null,"abstract":"<p>We read with great interest the article by Lu et al. [<span>1</span>] regarding the impact of myosteatosis on post–liver transplantation (LT) outcome in males transplanted for hepatocellular carcinoma (HCC). The authors reported a relatively low prevalence of myosteatosis (27.8% in males) using a gender-based definition (i.e., muscle attenuation less than 37.5 HU at the third lumbar vertebra of cross-sectional CT image for men). However, in our recently published meta-analysis [<span>2</span>] including 10 studies with 3316 HCC patients, the overall pooled prevalence of myosteatosis was estimated as high as 50% (95% confidence interval [CI] 35%–65%) [<span>2</span>]. This discrepancy could be attributed to the fact that Lu et al. [<span>1</span>] included mainly chronic hepatitis B–associated HCC patients, although all patients were Asians. Indeed, our meta-analysis showed that the prevalence of myosteatosis is significantly lower in Asian HCC patients, compared to the non-Asian HCC patients (pooled prevalence 45% vs. 69%, respectively, <i>p</i> = 0.02), whereas viral-associated HCC patients have significantly less frequently myosteatosis, compared to those with fatty or alcoholic liver disease–associated HCC (pooled prevalence 49% vs. 65% vs. 86%, respectively, <i>p</i> < 0.001). Interestingly, the authors [<span>1</span>] concluded that myosteatosis was not associated with post-LT outcome in females, although they did not provide which cutoff was used for definition of myosteatosis in this subgroup, although no clear explanation was given for this finding. In addition, they found no association between myosteatosis and hepatic encephalopathy although our meta-analysis [<span>3</span>] showed that cirrhotic patients with myosteatosis, compared to those without myosteatosis, have more frequently a previous history of hepatic encephalopathy (32% vs. 15%, <i>p</i> = 0.04) possibly related with the reduction of skeletal muscle capacity to remove ammonia. Finally, it would be interesting if the authors evaluated the impact of diabetes mellitus, which is an known factor associated with myosteatosis and poor prognosis after LT [<span>3, 4</span>], as well as if they compared the post-LT outcome of HCC patients with sarcopenia and myosteatosis/isolated myosteatosis versus those with isolated sarcopenia, as recent studies have shown that myosteatosis may be a more important factor, compared to sarcopenia, in the pre-LT setting of patients without HCC [<span>5</span>].</p>\u0000<p>Nevertheless, Lu et al. [<span>1</span>] confirmed the predictive role of myosteatosis in HCC patients not only in the pre-LT setting [<span>2</span>] but also in the post-LT outcome [<span>1</span>], indicating the importance of including assessment of myosteatosis in the process for LT evaluation. However, their results [<span>1</span>] need validation in non-Asian populations, in which the aetiology of liver disease is more frequently metabolic and alcohol-related HCC.</p>","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ross A. Jones, Abdullah Ramadan, Shahd Qutifan, Thomas H. Gillingwater
<p>We read with interest the paper entitled ‘Neuromuscular impairment at different stages of human sarcopenia’ by Sarto et al. [<span>1</span>], which has used a variety of assessment approaches to innovatively investigate neuromuscular impairment in older human subjects. This study undoubtedly represents an important contribution to our understanding of the impact of age and sarcopenia on the human neuromuscular system, for which we wish to congratulate and thank the authors.</p> <p>Although the authors have presented a lot of important new data, they state in their conclusions that ‘an altered innervation profile and NMJ instability are prominent features of the ageing of the neuromuscular system’. This is based on the claim that an increase in neural cell adhesion molecule-positive fibres is evidence of ‘increased muscle denervation’. We would like to raise caution against such a conclusion when based on the type of indirect data presented by Sarto et al. [<span>1</span>].</p> <p>The term ‘muscle denervation’ refers to a specific process whereby the nerve supply (innervation) of a muscle fibre, derived from a lower motor neuron input, is removed or lost. For this term to be accurate, therefore, it requires evidence showing that lower motor neuron inputs at the NMJ are removed or lost. We would politely suggest that an increase in neural cell adhesion molecule-positive fibres is not such evidence. Rather, anatomical and morphological studies of the NMJ are required to be able to draw such conclusions.</p> <p>Sarto et al. [<span>1</span>] point out in their paper that morphological evidence for NMJ disruption, and hence muscle denervation, is present in rodent models of ageing [<span>2</span>] and use this to support their claims in humans. However, whilst technically challenging, comparable morphological studies of NMJs in young and old humans have been performed, showing that, in stark contrast to rodent models, NMJs remain structurally intact over the normal human lifespan [<span>3</span>]. Such species-specific differences are perhaps not surprising given the inherent differences that exist in NMJ structure and stability between rodents and humans [<span>4, 5</span>]. As such, the strongest <i>direct</i> evidence available to date suggests that motor neuron inputs at the NMJ are not removed or lost with increasing age in humans. This in no way precludes the possibility that age- and/or sarcopenia-related changes, such as those reported by Sarto et al., [<span>1</span>] are occurring in muscle that mimic denervation-induced changes. Rather, it questions the premise that such changes are occurring due to a loss of innervation resulting from structural breakdown of the NMJ.</p> <p>The use of indirect measurements to draw conclusions about NMJ status and muscle denervation is not an issue solely restricted to Sarto et al.'s paper [<span>1</span>], and we by no means wish to single out this important study in this regard (indeed, we strongly welc
{"title":"Comment on ‘Neuromuscular Impairment at Different Stages of Human Sarcopenia’ by Sarto et al.","authors":"Ross A. Jones, Abdullah Ramadan, Shahd Qutifan, Thomas H. Gillingwater","doi":"10.1002/jcsm.13624","DOIUrl":"https://doi.org/10.1002/jcsm.13624","url":null,"abstract":"<p>We read with interest the paper entitled ‘Neuromuscular impairment at different stages of human sarcopenia’ by Sarto et al. [<span>1</span>], which has used a variety of assessment approaches to innovatively investigate neuromuscular impairment in older human subjects. This study undoubtedly represents an important contribution to our understanding of the impact of age and sarcopenia on the human neuromuscular system, for which we wish to congratulate and thank the authors.</p>\u0000<p>Although the authors have presented a lot of important new data, they state in their conclusions that ‘an altered innervation profile and NMJ instability are prominent features of the ageing of the neuromuscular system’. This is based on the claim that an increase in neural cell adhesion molecule-positive fibres is evidence of ‘increased muscle denervation’. We would like to raise caution against such a conclusion when based on the type of indirect data presented by Sarto et al. [<span>1</span>].</p>\u0000<p>The term ‘muscle denervation’ refers to a specific process whereby the nerve supply (innervation) of a muscle fibre, derived from a lower motor neuron input, is removed or lost. For this term to be accurate, therefore, it requires evidence showing that lower motor neuron inputs at the NMJ are removed or lost. We would politely suggest that an increase in neural cell adhesion molecule-positive fibres is not such evidence. Rather, anatomical and morphological studies of the NMJ are required to be able to draw such conclusions.</p>\u0000<p>Sarto et al. [<span>1</span>] point out in their paper that morphological evidence for NMJ disruption, and hence muscle denervation, is present in rodent models of ageing [<span>2</span>] and use this to support their claims in humans. However, whilst technically challenging, comparable morphological studies of NMJs in young and old humans have been performed, showing that, in stark contrast to rodent models, NMJs remain structurally intact over the normal human lifespan [<span>3</span>]. Such species-specific differences are perhaps not surprising given the inherent differences that exist in NMJ structure and stability between rodents and humans [<span>4, 5</span>]. As such, the strongest <i>direct</i> evidence available to date suggests that motor neuron inputs at the NMJ are not removed or lost with increasing age in humans. This in no way precludes the possibility that age- and/or sarcopenia-related changes, such as those reported by Sarto et al., [<span>1</span>] are occurring in muscle that mimic denervation-induced changes. Rather, it questions the premise that such changes are occurring due to a loss of innervation resulting from structural breakdown of the NMJ.</p>\u0000<p>The use of indirect measurements to draw conclusions about NMJ status and muscle denervation is not an issue solely restricted to Sarto et al.'s paper [<span>1</span>], and we by no means wish to single out this important study in this regard (indeed, we strongly welc","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
I have read with great interest the article published in the Journal of Cachexia, Sarcopenia and Muscle on the knowledge and practices in anorexia of ageing (AA) diagnosis and management in Japan [1]. The study provides valuable insights into the current state of AA management among healthcare professionals in Japan, emphasizing the critical role of continuing education. While the article is well written and contributes meaningfully to the field, I believe there are several areas where constructive suggestions could further enhance the interpretation and application of the results.
From a statistical perspective, the study has some limitations that merit consideration. The use of descriptive statistics and chi-square tests to compare differences between the education and non-education groups is commendable. However, incorporating multivariable regression models could make the analysis even more insightful, as these models would effectively control for potential confounding factors such as participants' work experience, institutional resources and overall attitudes towards elderly care. Additionally, examining interaction effects could significantly enhance the persuasiveness of the study's findings. Education may impact the management of AA differently across various professions, regions or institutions. Considering these interaction effects within the statistical models would provide a deeper understanding of how these factors collectively influence the results [2].
To address the challenges highlighted by this study, I propose a multidisciplinary approach involving community health initiatives. A coordinated effort that includes healthcare providers, community health workers, social workers and government officials could create a more supportive environment for managing AA. For example, community-based nutrition education programmes could be developed to reach a broader audience, including those outside academic settings. Additionally, leveraging the role of community health workers to monitor and manage AA in older adults could enhance early detection and intervention [3], particularly in underserved areas.
In conclusion, while the article offers valuable contributions to understanding AA management in Japan, our suggestions aim to make an already excellent article even better. I look forward to seeing continued efforts from healthcare professionals, volunteers, government officials and social workers to create a healthier and more supportive environment for older adults.
我饶有兴趣地阅读了发表在 Journal of Cachexia, Sarcopenia and Muscle 上的一篇关于日本老年厌食症（AA）诊断和管理的知识与实践的文章[1]。该研究为了解日本医护人员在老年性厌食症管理方面的现状提供了宝贵的见解，强调了继续教育的关键作用。虽然文章写得很好，对该领域做出了有意义的贡献，但我认为有几个方面的建设性建议可以进一步加强对结果的解释和应用。使用描述性统计和卡方检验来比较教育组和非教育组之间的差异是值得称赞的。但是，如果采用多变量回归模型，可以使分析更有洞察力，因为这些模型可以有效控制潜在的干扰因素，如参与者的工作经验、机构资源和对老年人护理的总体态度。此外，研究交互效应也能大大增强研究结果的说服力。教育可能会对不同职业、地区或机构的 AA 管理产生不同的影响。在统计模型中考虑这些交互效应，可以更深入地了解这些因素是如何共同影响研究结果的[2]。包括医疗服务提供者、社区卫生工作者、社会工作者和政府官员在内的协调努力可以为管理 AA 创造一个更有利的环境。例如，可以制定以社区为基础的营养教育计划，以扩大受众范围，包括学术环境之外的受众。此外，利用社区卫生工作者在监测和管理老年人 AA 方面的作用，可以加强早期发现和干预[3]，尤其是在服务不足的地区。总之，虽然这篇文章为了解日本的 AA 管理做出了宝贵贡献，但我们的建议旨在使这篇已经非常出色的文章更加完美。我期待看到医护人员、志愿者、政府官员和社会工作者继续努力，为老年人创造一个更健康、更有支持性的环境。
{"title":"Comment on ‘Survey on the Knowledge and Practices in Anorexia of Aging Diagnosis and Management in Japan’ by Takagi et al.","authors":"Ying Cui","doi":"10.1002/jcsm.13626","DOIUrl":"https://doi.org/10.1002/jcsm.13626","url":null,"abstract":"<p>I have read with great interest the article published in the <i>Journal of Cachexia, Sarcopenia and Muscle</i> on the knowledge and practices in anorexia of ageing (AA) diagnosis and management in Japan [<span>1</span>]. The study provides valuable insights into the current state of AA management among healthcare professionals in Japan, emphasizing the critical role of continuing education. While the article is well written and contributes meaningfully to the field, I believe there are several areas where constructive suggestions could further enhance the interpretation and application of the results.</p>\u0000<p>From a statistical perspective, the study has some limitations that merit consideration. The use of descriptive statistics and chi-square tests to compare differences between the education and non-education groups is commendable. However, incorporating multivariable regression models could make the analysis even more insightful, as these models would effectively control for potential confounding factors such as participants' work experience, institutional resources and overall attitudes towards elderly care. Additionally, examining interaction effects could significantly enhance the persuasiveness of the study's findings. Education may impact the management of AA differently across various professions, regions or institutions. Considering these interaction effects within the statistical models would provide a deeper understanding of how these factors collectively influence the results [<span>2</span>].</p>\u0000<p>To address the challenges highlighted by this study, I propose a multidisciplinary approach involving community health initiatives. A coordinated effort that includes healthcare providers, community health workers, social workers and government officials could create a more supportive environment for managing AA. For example, community-based nutrition education programmes could be developed to reach a broader audience, including those outside academic settings. Additionally, leveraging the role of community health workers to monitor and manage AA in older adults could enhance early detection and intervention [<span>3</span>], particularly in underserved areas.</p>\u0000<p>In conclusion, while the article offers valuable contributions to understanding AA management in Japan, our suggestions aim to make an already excellent article even better. I look forward to seeing continued efforts from healthcare professionals, volunteers, government officials and social workers to create a healthier and more supportive environment for older adults.</p>","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mikel L Sáez de Asteasu,Nicolás Martínez-Velilla,Fabricio Zambom-Ferraresi,Yesenia García-Alonso,Arkaitz Galbete,Robinson Ramírez-Vélez,Eduardo L Cadore,Mikel Izquierdo
BACKGROUNDHospitalization exacerbates sarcopenia and physical dysfunction in older adults. Whether tailored inpatient exercise prevents acute sarcopenia is unknown. This study aimed to examine the effect of a multicomponent exercise programme on muscle and physical function in hospitalized older adults. We hypothesized that participation in a brief tailored exercise regimen (i.e., 3-5 days) would attenuate muscle function and structure changes compared with usual hospital care alone.METHODSThis randomized clinical trial with blinded outcome assessment was conducted from May 2018 to April 2021 at Hospital Universitario de Navarra, Spain. Participants were 130 patients aged 75 years and older admitted to an acute care geriatric unit. Patients were randomized to a tailored 3- to 5-day exercise programme (n = 64) or usual hospital care (control, n = 66) consisting of physical therapy if needed. The coprimary endpoints were between-group differences in changes in short physical performance battery (SPPB) score and usual gait velocity from hospital admission to discharge. Secondary endpoints included changes in rectus femoris echo intensity, cross-sectional area, thickness and subcutaneous and intramuscular fat by ultrasound.RESULTSAmong 130 randomized patients (mean [SD] age, 87.7 [4.6] years; 57 [44%] women), the exercise group increased their mean SPPB score by 0.98 points (95% CI, 0.28-1.69 points) and gait velocity by 0.09 m/s (95% CI, 0.03-0.15 m/s) more than controls (both p < 0.01). No between-group differences were observed in any ultrasound muscle outcomes. There were no study-related adverse events.CONCLUSIONSThree to 5 days of tailored multicomponent exercise provided functional benefits but did not alter muscle or fat architecture compared with usual hospital care alone among vulnerable older patients. Brief exercise may help prevent acute sarcopenia during hospitalization.TRIAL REGISTRATIONClinicalTrials.gov identifier: NCT04600453.
{"title":"Short-Term Multicomponent Exercise Impact on Muscle Function and Structure in Hospitalized Older at Risk of Acute Sarcopenia.","authors":"Mikel L Sáez de Asteasu,Nicolás Martínez-Velilla,Fabricio Zambom-Ferraresi,Yesenia García-Alonso,Arkaitz Galbete,Robinson Ramírez-Vélez,Eduardo L Cadore,Mikel Izquierdo","doi":"10.1002/jcsm.13602","DOIUrl":"https://doi.org/10.1002/jcsm.13602","url":null,"abstract":"BACKGROUNDHospitalization exacerbates sarcopenia and physical dysfunction in older adults. Whether tailored inpatient exercise prevents acute sarcopenia is unknown. This study aimed to examine the effect of a multicomponent exercise programme on muscle and physical function in hospitalized older adults. We hypothesized that participation in a brief tailored exercise regimen (i.e., 3-5 days) would attenuate muscle function and structure changes compared with usual hospital care alone.METHODSThis randomized clinical trial with blinded outcome assessment was conducted from May 2018 to April 2021 at Hospital Universitario de Navarra, Spain. Participants were 130 patients aged 75 years and older admitted to an acute care geriatric unit. Patients were randomized to a tailored 3- to 5-day exercise programme (n = 64) or usual hospital care (control, n = 66) consisting of physical therapy if needed. The coprimary endpoints were between-group differences in changes in short physical performance battery (SPPB) score and usual gait velocity from hospital admission to discharge. Secondary endpoints included changes in rectus femoris echo intensity, cross-sectional area, thickness and subcutaneous and intramuscular fat by ultrasound.RESULTSAmong 130 randomized patients (mean [SD] age, 87.7 [4.6] years; 57 [44%] women), the exercise group increased their mean SPPB score by 0.98 points (95% CI, 0.28-1.69 points) and gait velocity by 0.09 m/s (95% CI, 0.03-0.15 m/s) more than controls (both p < 0.01). No between-group differences were observed in any ultrasound muscle outcomes. There were no study-related adverse events.CONCLUSIONSThree to 5 days of tailored multicomponent exercise provided functional benefits but did not alter muscle or fat architecture compared with usual hospital care alone among vulnerable older patients. Brief exercise may help prevent acute sarcopenia during hospitalization.TRIAL REGISTRATIONClinicalTrials.gov identifier: NCT04600453.","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142436035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Obesity is a significant risk factor for the progression of non-alcoholic fatty liver disease (NAFLD). However, a convenient and efficacious non-invasive test for monitoring NAFLD progression in patients with obesity is currently lacking. This study aims to investigate the associations between CT-based body composition and the progression of biopsy-proven NAFLD in patients with obesity.
Methods: Liver biopsy was conducted in patients with obesity, and the progression of NAFLD was evaluated by the NAFLD activity score (NAS). Body composition was assessed through abdominal computed tomography (CT) scans.
Results: A total of 602 patients with an average age of 31.65 (±9.33) years old were included, comprising 217 male patients and 385 female patients. The wall skeletal muscle index (SMI), total SMI, and visceral fat index (VFI) were positively correlated with NAS in both male and female patients. Multivariate regression analysis demonstrated significant associations between high liver steatosis and wall SMI (HR: 1.60, 95% CI: 1.12 to 2.30), total SMI (HR: 1.50, 95% CI: 1.02 to 2.08), VSI (HR: 2.16, 95% CI: 1.48 to 3.14), visceral fat to muscle ratio (HR: 1.51, 95% CI: 1.05 to 2.18), and visceral to subcutaneous fat ratio (HR: 1.51, 95% CI: 1.07 to 2.12). Non-alcoholic steatohepatitis (NASH) was significantly associated with wall SMI (HR: 1.52, 95% CI: 1.06 to 2.19) and VSI (HR: 1.50, 95% CI: 1.03 to 2.17). Liver fibrosis ≥ F2 was significantly associated with psoas muscle index (HR: 0.64, 95% CI: 0.44 to 0.93) and psoas skeletal muscle density (HR: 0.61, 95% CI: 0.41 to 0.89).
Conclusions: Our study suggested that certain CT-based body composition indicators, notably high VFI, were significantly associated with the progression of NAFLD in patients with obesity. Great attentions and timely managements should be given to these patients with body composition characteristics associated with the risk of NAFLD progression.
{"title":"Body Composition and Progression of Biopsy-Proven Non-Alcoholic Fatty Liver Disease in Patients With Obesity.","authors":"Qianyi Wan, Xingzhu Liu, Jinghao Xu, Rui Zhao, Shiqin Yang, Jianrong Feng, Zhan Cao, Jingru Li, Xiaopeng He, Haiou Chen, Jinbao Ye, Haiyang Chen, Yi Chen","doi":"10.1002/jcsm.13605","DOIUrl":"https://doi.org/10.1002/jcsm.13605","url":null,"abstract":"<p><strong>Background: </strong>Obesity is a significant risk factor for the progression of non-alcoholic fatty liver disease (NAFLD). However, a convenient and efficacious non-invasive test for monitoring NAFLD progression in patients with obesity is currently lacking. This study aims to investigate the associations between CT-based body composition and the progression of biopsy-proven NAFLD in patients with obesity.</p><p><strong>Methods: </strong>Liver biopsy was conducted in patients with obesity, and the progression of NAFLD was evaluated by the NAFLD activity score (NAS). Body composition was assessed through abdominal computed tomography (CT) scans.</p><p><strong>Results: </strong>A total of 602 patients with an average age of 31.65 (±9.33) years old were included, comprising 217 male patients and 385 female patients. The wall skeletal muscle index (SMI), total SMI, and visceral fat index (VFI) were positively correlated with NAS in both male and female patients. Multivariate regression analysis demonstrated significant associations between high liver steatosis and wall SMI (HR: 1.60, 95% CI: 1.12 to 2.30), total SMI (HR: 1.50, 95% CI: 1.02 to 2.08), VSI (HR: 2.16, 95% CI: 1.48 to 3.14), visceral fat to muscle ratio (HR: 1.51, 95% CI: 1.05 to 2.18), and visceral to subcutaneous fat ratio (HR: 1.51, 95% CI: 1.07 to 2.12). Non-alcoholic steatohepatitis (NASH) was significantly associated with wall SMI (HR: 1.52, 95% CI: 1.06 to 2.19) and VSI (HR: 1.50, 95% CI: 1.03 to 2.17). Liver fibrosis ≥ F2 was significantly associated with psoas muscle index (HR: 0.64, 95% CI: 0.44 to 0.93) and psoas skeletal muscle density (HR: 0.61, 95% CI: 0.41 to 0.89).</p><p><strong>Conclusions: </strong>Our study suggested that certain CT-based body composition indicators, notably high VFI, were significantly associated with the progression of NAFLD in patients with obesity. Great attentions and timely managements should be given to these patients with body composition characteristics associated with the risk of NAFLD progression.</p>","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142398843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhibo Deng, Chao Song, Long Chen, Rongsheng Zhang, Linhai Yang, Peng Zhang, Yu Xiu, Yibin Su, Fenqi Luo, Jun Luo, Hanhao Dai, Jie Xu
<p><strong>Background: </strong>Skeletal muscle is the primary organ involved in insulin-mediated glucose metabolism. Elevated levels of CILP2 are a significant indicator of impaired glucose tolerance and are predominantly expressed in skeletal muscle. It remains unclear whether CILP2 contributes to age-related muscle atrophy through regulating the glucose homeostasis and insulin sensitivity.</p><p><strong>Methods: </strong>Initially, the expression levels of CILP2 were assessed in elderly mice and patients with sarcopenia. Lentiviral vectors were used to induce either silencing or overexpression of CILP2 in C2C12 myoblast cells. The effects of CILP2 on proliferation, myogenic differentiation, insulin sensitivity and glucose uptake were evaluated using immunofluorescence, western blotting, real-time quantitative polymerase chain reaction, RNA sequencing, glucose uptake experiments, dual-luciferase reporter assays and co-immunoprecipitation (CO-IP). An adeno-associated virus-9 containing a muscle-specific promoter was injected into SAMP8 senile mice to observe the efficacy of CILP2 knockout.</p><p><strong>Results: </strong>We found that there was more CLIP2 expressed in the skeletal muscle of ageing mice (+1.1-fold, p < 0.01) and in patients with sarcopenia (+2.5-fold, p < 0.01) compared to the control group. Following the overexpression of CILP2, Ki67 (-65%, p < 0.01), PCNA (-32%, p < 0.05), MyoD1 (-89%, p < 0.001), MyoG (-31%, p < 0.05) and MyHC (-85%, p < 0.001), which indicate proliferation and differentiation potential, were significantly reduced. In contrast, MuRF-1 (+59%, p < 0.05), atrogin-1 (+43%, p < 0.05) and myostatin (+31%, p < 0.05), the markers of muscular atrophy, were significantly increased. Overexpression of CILP2 decreased insulin sensitivity, glucose uptake (-18%, p < 0.001), GLUT4 translocation to the membrane and the maximum respiratory capacity of mitochondria. Canonical Wnt signalling was identified through RNA sequencing as a potential pathway for CILP2 regulation in C2C12, and Wnt3a was confirmed as an interacting protein of CILP2 in the CO-IP assay. The addition of recombinant Wnt3a protein reversed the inhibitory effects on myogenesis and glucose metabolism caused by CILP2 overexpression. Conversely, CILP2 knockdown promoted myogenesis and glucose metabolism. CILP2 knockdown improved muscle atrophy in mice, characterized by significant increases in time to exhaustion (+42%, p < 0.001), grip strength (+19%, p < 0.01), muscle mass (+15%, p < 0.001) and mean muscle cross-sectional area (+37%, p < 0.01). CILP2 knockdown enhanced glycogen synthesis (+83%, p < 0.001) and the regeneration of oxidative and glycolytic muscle fibres in SAMP8 ageing mice via the Wnt/β-catenin signalling pathway.</p><p><strong>Conclusions: </strong>Our results indicate that CILP2 interacts with Wnt3a to suppress the Wnt/β-catenin signalling pathway and its downstream cascade, leading to impaired insulin sensitivity and glucose metabolism in skelet
{"title":"Inhibition of CILP2 Improves Glucose Metabolism and Mitochondrial Dysfunction in Sarcopenia via the Wnt Signalling Pathway.","authors":"Zhibo Deng, Chao Song, Long Chen, Rongsheng Zhang, Linhai Yang, Peng Zhang, Yu Xiu, Yibin Su, Fenqi Luo, Jun Luo, Hanhao Dai, Jie Xu","doi":"10.1002/jcsm.13597","DOIUrl":"https://doi.org/10.1002/jcsm.13597","url":null,"abstract":"<p><strong>Background: </strong>Skeletal muscle is the primary organ involved in insulin-mediated glucose metabolism. Elevated levels of CILP2 are a significant indicator of impaired glucose tolerance and are predominantly expressed in skeletal muscle. It remains unclear whether CILP2 contributes to age-related muscle atrophy through regulating the glucose homeostasis and insulin sensitivity.</p><p><strong>Methods: </strong>Initially, the expression levels of CILP2 were assessed in elderly mice and patients with sarcopenia. Lentiviral vectors were used to induce either silencing or overexpression of CILP2 in C2C12 myoblast cells. The effects of CILP2 on proliferation, myogenic differentiation, insulin sensitivity and glucose uptake were evaluated using immunofluorescence, western blotting, real-time quantitative polymerase chain reaction, RNA sequencing, glucose uptake experiments, dual-luciferase reporter assays and co-immunoprecipitation (CO-IP). An adeno-associated virus-9 containing a muscle-specific promoter was injected into SAMP8 senile mice to observe the efficacy of CILP2 knockout.</p><p><strong>Results: </strong>We found that there was more CLIP2 expressed in the skeletal muscle of ageing mice (+1.1-fold, p < 0.01) and in patients with sarcopenia (+2.5-fold, p < 0.01) compared to the control group. Following the overexpression of CILP2, Ki67 (-65%, p < 0.01), PCNA (-32%, p < 0.05), MyoD1 (-89%, p < 0.001), MyoG (-31%, p < 0.05) and MyHC (-85%, p < 0.001), which indicate proliferation and differentiation potential, were significantly reduced. In contrast, MuRF-1 (+59%, p < 0.05), atrogin-1 (+43%, p < 0.05) and myostatin (+31%, p < 0.05), the markers of muscular atrophy, were significantly increased. Overexpression of CILP2 decreased insulin sensitivity, glucose uptake (-18%, p < 0.001), GLUT4 translocation to the membrane and the maximum respiratory capacity of mitochondria. Canonical Wnt signalling was identified through RNA sequencing as a potential pathway for CILP2 regulation in C2C12, and Wnt3a was confirmed as an interacting protein of CILP2 in the CO-IP assay. The addition of recombinant Wnt3a protein reversed the inhibitory effects on myogenesis and glucose metabolism caused by CILP2 overexpression. Conversely, CILP2 knockdown promoted myogenesis and glucose metabolism. CILP2 knockdown improved muscle atrophy in mice, characterized by significant increases in time to exhaustion (+42%, p < 0.001), grip strength (+19%, p < 0.01), muscle mass (+15%, p < 0.001) and mean muscle cross-sectional area (+37%, p < 0.01). CILP2 knockdown enhanced glycogen synthesis (+83%, p < 0.001) and the regeneration of oxidative and glycolytic muscle fibres in SAMP8 ageing mice via the Wnt/β-catenin signalling pathway.</p><p><strong>Conclusions: </strong>Our results indicate that CILP2 interacts with Wnt3a to suppress the Wnt/β-catenin signalling pathway and its downstream cascade, leading to impaired insulin sensitivity and glucose metabolism in skelet","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The splicing factor SRSF1 emerges as a mater regulator of cell proliferation, displaying high expression in actively proliferative satellite cells (SCs). In SRSF1 knockout mice (KO) generated via MyoD-Cre, early mortality and muscle atrophy are observed during postnatal muscle growth. Despite these findings, the precise mechanisms through which SRSF1 loss influences SCs' functions and its role in muscle regeneration remain to be elucidated.
{"title":"SRSF1 Is Crucial for Maintaining Satellite Cell Homeostasis During Skeletal Muscle Growth and Regeneration","authors":"Zhenzhen Wang, Qian Peng, Zhige Zhang, Xue You, Huimin Duan, Rula Sha, Ningyang Yuan, Zhigang Li, Zhiqin Xie, Jun Han, Ying Feng","doi":"10.1002/jcsm.13607","DOIUrl":"https://doi.org/10.1002/jcsm.13607","url":null,"abstract":"The splicing factor SRSF1 emerges as a mater regulator of cell proliferation, displaying high expression in actively proliferative satellite cells (SCs). In SRSF1 knockout mice (KO) generated via <i>MyoD-Cre</i>, early mortality and muscle atrophy are observed during postnatal muscle growth. Despite these findings, the precise mechanisms through which SRSF1 loss influences SCs' functions and its role in muscle regeneration remain to be elucidated.","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142385712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BackgroundTraditional metrics such as body mass index (BMI) and waist circumference (WC) fail to accurately assess the health outcomes associated with abdominal adiposity, because they neglect the intricacies of adipose tissue distribution. Notably, the variability in body composition scaled to height remains underexplored in Chinese demographics. This study introduces height‐normalised indices of abdominal adiposity using computed tomography (CT) scans and further assesses their associations with various health outcomes.MethodsIn a large, diverse Chinese population (n = 1054 healthy individuals; n = 1159 with dyslipidemia; n = 803 with diabetes; n = 1289 with cardio‐cerebrovascular diseases; n = 1108 with cancers; and n = 509 with abnormal bone mas), abdominal CT scans were performed and allometric growth model analyses were used to derive height‐normalised indices (body composition/heightβ). Logistic regression models assessed the associations between these indices and health outcomes.ResultsDistinct scaling powers were observed for visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and total abdominal adipose tissue (TAT), as well as for sagittal diameter (SAD), with marked sex differences. Powers for VAT were 1.786 ± 1.270 for males and 1.274 ± 0.692 for females. Powers for SAT were 2.266 ± 0.856 for males and 1.656 ± 0.497 for females. Powers for TAT were 2.141 ± 0.967 for males and 1.438 ± 0.489 for females. Powers for SAD were 0.646 ± 0.217 for males and 0.678 ± 0.141 for females. After controlling for age, BMI and WC, VAT/heightβ, TAT/heightβ and SAD/heightβ retained their significantly positive associations with the odds of health outcomes, whereas SAT/heightβ did not.ConclusionsOur findings endorse the clinical utility of height‐normalised indices, particularly VAT/heightβ, TAT/heightβ and SAD/heightβ, in health outcomes assessment. These indices, grounded in robust empirical data, underscore the necessity of a nuanced approach in obesity‐related health evaluations, advocating for a departure from conventional methods like BMI.
{"title":"Evaluation of Health Associations With Height‐Normalised Abdominal Body Composition Indices: A Single‐Centre Cross‐Sectional Study","authors":"Yupeng Liu, Hangqian He, Keyu Qian, Yufeng Huang, Xuemei Ao, Xudong Shi, Binye Ruan, Ru Xue, Xiaoyi Fu, Shuran Wang","doi":"10.1002/jcsm.13609","DOIUrl":"https://doi.org/10.1002/jcsm.13609","url":null,"abstract":"BackgroundTraditional metrics such as body mass index (BMI) and waist circumference (WC) fail to accurately assess the health outcomes associated with abdominal adiposity, because they neglect the intricacies of adipose tissue distribution. Notably, the variability in body composition scaled to height remains underexplored in Chinese demographics. This study introduces height‐normalised indices of abdominal adiposity using computed tomography (CT) scans and further assesses their associations with various health outcomes.MethodsIn a large, diverse Chinese population (<jats:italic>n</jats:italic> = 1054 healthy individuals; <jats:italic>n</jats:italic> = 1159 with dyslipidemia; <jats:italic>n</jats:italic> = 803 with diabetes; <jats:italic>n</jats:italic> = 1289 with cardio‐cerebrovascular diseases; <jats:italic>n</jats:italic> = 1108 with cancers; and <jats:italic>n</jats:italic> = 509 with abnormal bone mas), abdominal CT scans were performed and allometric growth model analyses were used to derive height‐normalised indices (body composition/height<jats:sup><jats:italic>β</jats:italic></jats:sup>). Logistic regression models assessed the associations between these indices and health outcomes.ResultsDistinct scaling powers were observed for visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and total abdominal adipose tissue (TAT), as well as for sagittal diameter (SAD), with marked sex differences. Powers for VAT were 1.786 ± 1.270 for males and 1.274 ± 0.692 for females. Powers for SAT were 2.266 ± 0.856 for males and 1.656 ± 0.497 for females. Powers for TAT were 2.141 ± 0.967 for males and 1.438 ± 0.489 for females. Powers for SAD were 0.646 ± 0.217 for males and 0.678 ± 0.141 for females. After controlling for age, BMI and WC, VAT/height<jats:sup><jats:italic>β</jats:italic></jats:sup>, TAT/height<jats:sup><jats:italic>β</jats:italic></jats:sup> and SAD/height<jats:sup><jats:italic>β</jats:italic></jats:sup> retained their significantly positive associations with the odds of health outcomes, whereas SAT/height<jats:sup><jats:italic>β</jats:italic></jats:sup> did not.ConclusionsOur findings endorse the clinical utility of height‐normalised indices, particularly VAT/height<jats:sup><jats:italic>β</jats:italic></jats:sup>, TAT/height<jats:sup><jats:italic>β</jats:italic></jats:sup> and SAD/height<jats:sup><jats:italic>β</jats:italic></jats:sup>, in health outcomes assessment. These indices, grounded in robust empirical data, underscore the necessity of a nuanced approach in obesity‐related health evaluations, advocating for a departure from conventional methods like BMI.","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142384526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BackgroundDynapenic obesity is a condition characterized by high adiposity levels combined with muscle dysfunction. Although high adiposity and muscle loss/dysfunction are thought to synergistically increase the risk of cardiovascular disease (CVD), few studies have addressed the association between dynapenic and sarcopenic obesity and CVD. We aimed to investigate the association of dynapenic obesity with incident CVD events using the data from a population‐based prospective longitudinal study in Japan.MethodsA total of 2490 community‐dwelling Japanese aged 40–79 years (42.5% males, mean age 57.7 ± 10.6 years) without a history of CVD were followed up for a median of 24 years. Handgrip strength was classified as low, medium, or high by age‐ and sex‐specific tertiles. Body mass index (BMI) levels were categorized as lean (<18.5 kg/m2), normal (18.5–24.9 kg/m2), or obese (≥25.0 kg/m2). Dynapenic obesity was defined as having both low handgrip strength and obesity. The outcomes were defined as the first‐ever development of CVD (defined as stroke or coronary heart disease). The hazard ratios (HRs) and their 95% confidence intervals (CIs) for the development of CVD were estimated using a Cox proportional hazards model, in which participants with high handgrip strength and normal BMI were used as a reference group. Mediation analyses used serum high‐sensitivity C‐reactive protein (hs‐CRP) and homeostatic model assessment for insulin resistance (HOMA‐IR) as mediators.ResultsDuring the follow‐up period, 482 participants developed CVD events (324 cases of stroke and 209 of coronary heart disease). The multivariable‐adjusted risk of CVD increased significantly among participants with dynapenic obesity compared with the reference group (HR 1.49, 95% CI 1.03–2.17). An analysis by age groups showed a further increase in the risk of CVD among participants with dynapenic obesity aged less than 65 years (HR 1.66, 95% CI 1.04–2.65). In mediation analyses for participants aged less than 65 years, serum hs‐CRP was shown to be a significant mediator explaining 13.8% of the association between dynapenic obesity and the development of CVD, while HOMA‐IR explained 12.2% of this relationship.ConclusionsDynapenic obesity was a significant risk factor for the development of CVD in a general Japanese population. This association was more pronounced among those aged <65 years. Inflammation, and possibly glucose metabolism, might partly mediate this association. Our findings suggest that preventing muscle dysfunction as well as appropriate weight control, especially in middle‐age, are important for preventing the development of CVD.
{"title":"Association between dynapenic obesity and risk of cardiovascular disease: The Hisayama study","authors":"Yu Setoyama, Takanori Honda, Takahiro Tajimi, Satoko Sakata, Emi Oishi, Yoshihiko Furuta, Mao Shibata, Jun Hata, Takanari Kitazono, Yasuharu Nakashima, Toshiharu Ninomiya","doi":"10.1002/jcsm.13564","DOIUrl":"https://doi.org/10.1002/jcsm.13564","url":null,"abstract":"BackgroundDynapenic obesity is a condition characterized by high adiposity levels combined with muscle dysfunction. Although high adiposity and muscle loss/dysfunction are thought to synergistically increase the risk of cardiovascular disease (CVD), few studies have addressed the association between dynapenic and sarcopenic obesity and CVD. We aimed to investigate the association of dynapenic obesity with incident CVD events using the data from a population‐based prospective longitudinal study in Japan.MethodsA total of 2490 community‐dwelling Japanese aged 40–79 years (42.5% males, mean age 57.7 ± 10.6 years) without a history of CVD were followed up for a median of 24 years. Handgrip strength was classified as low, medium, or high by age‐ and sex‐specific tertiles. Body mass index (BMI) levels were categorized as lean (<18.5 kg/m<jats:sup>2</jats:sup>), normal (18.5–24.9 kg/m<jats:sup>2</jats:sup>), or obese (≥25.0 kg/m<jats:sup>2</jats:sup>). Dynapenic obesity was defined as having both low handgrip strength and obesity. The outcomes were defined as the first‐ever development of CVD (defined as stroke or coronary heart disease). The hazard ratios (HRs) and their 95% confidence intervals (CIs) for the development of CVD were estimated using a Cox proportional hazards model, in which participants with high handgrip strength and normal BMI were used as a reference group. Mediation analyses used serum high‐sensitivity C‐reactive protein (hs‐CRP) and homeostatic model assessment for insulin resistance (HOMA‐IR) as mediators.ResultsDuring the follow‐up period, 482 participants developed CVD events (324 cases of stroke and 209 of coronary heart disease). The multivariable‐adjusted risk of CVD increased significantly among participants with dynapenic obesity compared with the reference group (HR 1.49, 95% CI 1.03–2.17). An analysis by age groups showed a further increase in the risk of CVD among participants with dynapenic obesity aged less than 65 years (HR 1.66, 95% CI 1.04–2.65). In mediation analyses for participants aged less than 65 years, serum hs‐CRP was shown to be a significant mediator explaining 13.8% of the association between dynapenic obesity and the development of CVD, while HOMA‐IR explained 12.2% of this relationship.ConclusionsDynapenic obesity was a significant risk factor for the development of CVD in a general Japanese population. This association was more pronounced among those aged <65 years. Inflammation, and possibly glucose metabolism, might partly mediate this association. Our findings suggest that preventing muscle dysfunction as well as appropriate weight control, especially in middle‐age, are important for preventing the development of CVD.","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":null,"pages":null},"PeriodicalIF":8.9,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142385471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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