Diagnostic Criteria and Clinical Outcomes in Sarcopenia Research: A Literature Review

Han, Alex; Bokshan, Steven L.; Marcaccio, Stephen; DePasse, J. Mason; Daniels, Alan H.

doi:10.3390/jcm7040070

Cited by 83 publications

(70 citation statements)

References 46 publications

(64 reference statements)

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“…The presence of focal fatty infiltration was not sufficient by itself to define steatosis. Muscle mass was assessed from CT using the psoas muscle index (PMI), calculated by the area of the psoas muscles at the level of L3 divided by the height squared …”

Section: Methodsmentioning

confidence: 99%

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Development of Hepatic Steatosis After Chemotherapy for Non‐Hodgkin Lymphoma

et al. 2018

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Nonalcoholic fatty liver disease is the most common liver disorder in the developed world. Although typically reflecting caloric overload, it can also be secondary to drug toxicity. We aimed to describe the incidence and risk factors for de novo steatosis during chemotherapy for non‐Hodgkin lymphoma (NHL). In this retrospective case‐control study, adult patients with NHL were treated with rituximab, cyclophosphamide, doxorubicin, prednisone, and vincristine (R‐CHOP) or R‐CHOP + etoposide (EPOCH‐R). Patients with liver disease or steatosis were excluded. Abdominal computed tomography was performed pretreatment and at 3‐ to 6‐month intervals and reviewed for steatosis. Patients with de novo steatosis were matched 1:1 to controls by age, sex, and ethnicity. Of 251 treated patients (median follow‐up 53 months), 25 (10%) developed de novo steatosis, with the vast majority (23 of 25; 92%) developing it after chemotherapy. Of those, 14 (61%) developed steatosis within the first 18 months posttreatment and 20 (87%) within 36 months. Cases had higher baseline body mass index (BMI; mean ± SD, 29.0 ± 6.5 versus 26.0 ± 5.2 kg/m2; P = 0.014) and hyperlipidemia (12% versus 2%; P = 0.035). Although their weights did not change during chemotherapy, BMI in cases increased by 2.4 ± 2 kg/m2 (mean ± SD) from end of treatment to steatosis compared to 0.68 ± 1.4 in controls (P = 0.003). Etoposide‐containing regimens were associated with a shorter time to steatosis (median 34 weeks versus 154 weeks; P < 0.001) despite similar baseline risk factors. Conclusion: The recovery period from NHL chemotherapy appears to be a “hot spot” for development of fatty liver, driven by early posttreatment weight gain, especially in subjects with baseline risk factors.

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Section: Methodsmentioning

confidence: 99%

“…Muscle mass was assessed from CT using the psoas muscle index (PMI), calculated by the area of the psoas muscles at the level of L3 divided by the height squared. (13) aRtiCle inFoRmation:…”

Section: Radiologic Assessmentmentioning

confidence: 99%

Development of Hepatic Steatosis After Chemotherapy for Non‐Hodgkin Lymphoma

et al. 2018

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“…Muscle wasting occurs in response to a variety of physiological and pathological conditions and is highly detrimental to the human body . For example, elderly people are known to undergo a progressive loss of muscle mass, which is associated with reduced muscle force, decreased physical activity, insulin resistance, and increased risk of fracture . Progressive muscle wasting and weakness also occur in Duchenne muscular dystrophy (DMD), an inherited X‐linked recessive disorder caused by a mutation in the dystrophin gene.…”

Section: Introductionmentioning

confidence: 99%

Hemojuvelin is a novel suppressor for Duchenne muscular dystrophy and age‐related muscle wasting

Zhang

Wang

et al. 2019

J cachexia sarcopenia muscle

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Background Muscle wasting occurs in response to various physiological and pathological conditions, including ageing and Duchenne muscular dystrophy (DMD). Transforming growth factor‐β1 (TGF‐β1) contributes to muscle pathogenesis in elderly people and DMD patients; inhibition of TGF‐β1 signalling is a promising therapeutic strategy for muscle‐wasting disorders. Hemojuvelin (HJV or Hjv as the murine homologue) is a membrane‐bound protein that is highly expressed in skeletal muscle, heart, and liver. In hepatic cells, Hjv acts as a coreceptor for bone morphogenetic protein, a TGF‐β subfamily member. The aim of this study was to investigate whether Hjv plays an essential role in muscle physiological and pathophysiological processes by acting as a coreceptor for TGF‐β1 signalling. Methods Conventional and conditional Hjv knockout mice as well as mdx and aged mice transfected with Hjv overexpression vector were used to study the role of Hjv in muscle physiology and pathophysiology. qRT‐PCR, western blotting, and immunohistochemistry examinations were conducted to evaluate gene, protein, and structural changes in vivo and in vitro . Exercise endurance was determined using treadmill running test, and muscle force was detected by an isometric transducer. RNA interference, immunoprecipitation, and dual‐luciferase reporter assays were utilized to explore the mechanism by which Hjv regulates TGF‐β1 signalling in skeletal muscle. Results Conventional and conditional Hjv knockout mice displayed muscle atrophy, fibrosis, reduced running endurance, and muscle force. HJV was significantly down‐regulated in the muscles of DMD patients ( n = 3, mean age: 11.7 ± 5.7 years) and mdx mice as well as in those of aged humans ( n = 10, 20% women, mean age: 75.1 ± 9.5 years) and mice. Overexpression of Hjv rescued dystrophic and age‐related muscle wasting. Unlike its function in hepatic cells, the bone morphogenetic protein downstream phosphorylated p‐Smad1/5/8 signalling pathway was unchanged, but TGF‐β1, TGF‐β receptor II (TβRII), and p‐Smad2/3 expression were increased in Hjv‐ deficient muscles. Mechanistically, loss of Hjv promoted activation of Smad3 signalling induced by TGF‐β1, whereas Hjv overexpression inhibited TGF‐β1/Smad3 signalling by directly interacting with TβRII on the muscle membrane. Conclusions Our findings identify an unrecognized role of HJV in skeletal muscle by regulating TGF‐β1/Smad3 signalling as a coreceptor for TβRII. Unlike the TGF‐β1/Smad3 pathway, HJV could be a reliable drug target as its expression is not widespread. Novel therapeutic strategies could potentially be devised to interfere only with the muscle function of HJV to treat DMD and age‐re...

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“…Grip strength value of N/kg< 9 was considered as the threshold for sarcopenia in the SAR-model group. The recently described criteria for the diagnosis of sarcopenia include low muscle mass, which is an important causative factor, followed by low muscle strength and poor physical performance (Cruz-Jentoft et al, 2010;Han, Bokshan, Marcaccio, DePasse, & Daniels, 2018).…”

Section: Discussionmentioning

confidence: 99%

Physical activity improves sarcopenia in a murine model by enhancing the proliferative potential of muscle stem cells, oxidative capacity of mitochondrial enzymes and expression of Sestrins

Anwar

Mallick

Paliwal

et al. 2019

Preprint

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Sarcopenia is a major health issue in old age. Underlying molecular mechanisms in its genesis remain unclear and optimal animal models are yet to be established. A novel animal model was developed to identify structural and functional changes in skeletal muscles from sarcopenia. The influence of physical activity on animals of the sarcopenic model with respect to the expression of anti-oxidant proteins, mitochondrial oxidative capacity, and effect on muscle stem cells (MuSCs), were assessed. Male C57Bl/6 mice of different age groups were recruited: Y-Cntrl (young-control), A-Cntrl (agedcontrol), SAR-model and SAR-INT. SAR-model group was kept in a retrofitted confined cage and was fed with customized protein-restricted diet (14% protein), which is considered as a sarcopenic featured model. SAR-INT served as the intervention group. Three parameters, namely, muscle mass, grip strength, and physical endurance, were used to confirm the sarcopenic state. All physical parameters deteriorated most in SAR-model and it improved in the SAR-INT group. The impact of physical activity on the SAR-INT group was also evidenced by the improved proliferative potential of MuSCs determined by flow cytometric analysis. Compared with the SAR-model, the SAR-INT exhibited significant improvement in the oxidative capacity of mitochondrial enzymes and increased expression of anti-oxidant proteins, sestrins. In conclusion, physical activity improved physical parameters, MuSC proliferative potential, mitochondrial enzyme oxidative capacity and sestrin expression in sarcopenic animals. Hence, SAR-model in mice can serve as a novel sarcopenic model, physical activity provides scope for improvement in sarcopenic population and sestrin molecule can have a potential implication on sarcopenia.

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Diagnostic Criteria and Clinical Outcomes in Sarcopenia Research: A Literature Review

Cited by 83 publications

References 46 publications

Development of Hepatic Steatosis After Chemotherapy for Non‐Hodgkin Lymphoma

Development of Hepatic Steatosis After Chemotherapy for Non‐Hodgkin Lymphoma

Hemojuvelin is a novel suppressor for Duchenne muscular dystrophy and age‐related muscle wasting

Physical activity improves sarcopenia in a murine model by enhancing the proliferative potential of muscle stem cells, oxidative capacity of mitochondrial enzymes and expression of Sestrins

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