Oral Drugs Related with Muscle Wasting and Sarcopenia. A Review

Campins, Lluís; Camps, M. Valero; Riera, Ariadna; Pleguezuelos, Eulogio; Yébenes, Juan Carlos; Serra‐Prat, Mateu

doi:10.1159/000448247

Cited by 89 publications

(80 citation statements)

References 85 publications

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“…Finally, regarding the number of medications, this reflects the patient's comorbidity burden (more medications indicate more co-morbidities). The accumulation of diseases and other clinical deficits is very much part of the very concept of frailty [8,22]; nonetheless, since, in our study, the number of medications showed an independent effect in the multivariate model, the possibility cannot be ruled out that certain medications or drug interactions could predispose individuals to frailty [23].…”

Section: Discussionmentioning

confidence: 54%

Incidence and Risk Factors for Frailty in the Community-Dwelling Elderly Population. A Two-Year Follow-Up Cohort Study

Serra‐Prat¹,

Papiol²,

Vico³

et al. 2017

J Gerontol Geriatr Res

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Section: Discussionmentioning

confidence: 54%

Incidence and Risk Factors for Frailty in the Community-Dwelling Elderly Population. A Two-Year Follow-Up Cohort Study

Serra‐Prat¹,

Papiol²,

Vico³

et al. 2017

J Gerontol Geriatr Res

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“…However, our multivariate analysis showed that the number of medications had an independent effect on muscle strength; this would suggest that some medications may have an effect on muscle, as has also been suggested by a review on this topic [32]. Again, further studies are needed to explore in more detail the potential impact of certain medications on muscle wasting.…”

Section: Citationsupporting

confidence: 53%

Factors Associated with Poor Muscle Mass and Strength in A Community-Dwelling Elderly Population: A Cross-Sectional Study

Serra‐Prat¹,

Papiol²,

Vico³

et al. 2017

J Gerontol Geriatr Res

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IntroductionA progressive loss of muscle mass occurs from approximately 40 years of age. This loss has been estimated at about 8% per decade until the age of 70 years, after which the loss increases to 15% per decade [1]. Loss of muscle mass accompanied by loss of muscle strength or function is known as sarcopenia [2], a devastating geriatric syndrome leading to frailty, functional decline, disability, falls and even death [3,4]. Muscle mass and function, the main components of the frailty phenotype proposed by Fried [5], are a main determinant of physical performance and quality of life. The pathophysiology of muscle wasting in the older population is multifactorial and not completely understood [6]. Poor physical exercise and poor nutritional status are considered to be the main risk factors for sarcopenia. Other factors such as an imbalance between anabolic and catabolic hormones [7], metabolic disorders and insulin resistance [8] and chronic proinflammatory states have been associated with muscle wasting [9]. However, the specific role of each of these factors in the development of sarcopenia is not well known. Moreover, gender differences exist not only in body composition, muscle mass and strength but also in the prevalence of frailty and disability [10]. Older women are more prone to experiencing accelerated functional decline, and although they live longer than men they usually have a poorer quality of life [11]. These data would suggest that the pathophysiology of sarcopenia and frailty and the role of the above-mentioned risk factors may differ in men and women. A profound knowledge of the mechanisms involved in muscle wasting and sarcopenia is essential to the design of effective preventive measures to reduce both incidence and consequences. We hypothesize that low physical activity, obesity, inflammation and hormonal misbalances are associated with low muscle mass and strength. The aim of this study was to assess the main factors associated with poor muscle mass and strength in a community-dwelling elderly population and to assess differences by sex. Methods Study design and populationAn observational cross-sectional study was performed of community-dwelling adults aged 75 years and older. A sample was randomly selected from the database of 3 primary care centres in the municipalities of Mataró and Argentona (Barcelona, Spain). Individuals were excluded if they had active malignancy, dementia or serious mental illness, had a life expectancy of less than 6 months, were in a palliative care programme or were institutionalized. Persons who fulfilled all selection criteria and who signed the informed consent form were recruited from January to July 2014. The local ethics committee approved the study protocol (code 64/13). Details of the study design have been previously published [12]. AbstractBackground: The pathophysiology of muscle wasting in the elderly is multifactorial and not fully understood.

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“…Yang et al, 50 explained that Met activates the pathway involved in mitochondrial biogenesis and protects against apoptosis via the PGC-1α pathway. 51 22 Recently, Senesi et al, 29 indicated that Met regulates the principal molecular mediators of skeletal muscle hypertrophy and atrophy and is capable of inactivating the cellular mechanisms related to muscle injury.…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of metformin on muscle atrophy induced by obesity in rats

Hasan

Shalaby

El‐Gendy

et al. 2018

J of Cellular Biochemistry

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Aim A growing interest to understand the signaling pathways mediating obesity‐induced muscle atrophy is given. Metformin (Met) was reported to possess positive effects on preventing muscle damage and promoting muscle mass maintenance. The aim of the present study to investigate pathways involved in Met effect on obesity induced muscle atrophy. Methods Thirty adult male albino rats were assigned into two groups: normal chew diet fed group as control group (C; n = 10) and high‐fat‐diet (HFD) fed group ( n = 20). After 16 weeks, the HFD‐fed animals were subdivided into two groups; HFD group ( n = 10) and HFD fed treated with oral Met (320 mg/day) treatment (Met, n = 10) for 4 weeks. At the end of the experiment; final body weight, visceral fat weight, fasting blood glucose, insulin, lactate, total cholesterol, triglycerides were measured and calculated homeostatic model assessment insulin resistant (HOMA‐IR) for all groups. Soleus muscle weight, histopathlogical examination and expression of peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α), forkhead box O3 (FoxO3), atrogin‐1/MAFbx, and muscle RING finger 1 (MuRF‐1) were performed. Results HFD‐fed animals showed significant increase in final body weight, visceral fat mass, fasting blood glucose, insulin, calculated HOMA‐IR, lactate, total cholesterol and triglycerides with significant decrease in soleus muscle weight, PGC‐1α and significant increase in FoxO3, atrogin‐1/MAFbx, and MuRF‐1 expression. Also, there was significant decrease in fiber diameter, myosin heavy chain (MHC) I content while collagen content and myosin heavy chain IIa were increased compared with control group. Met‐treated group showed a significant decrease in the measured parameters compared with the HFD group. It also restored the gene expression, morphometric measures and MHC composition toward normal. Conclusion The current study is the first to provide evidence that Met could ameliorate muscle atrophy in high‐fat diet induced obesity and this effect may be in part due to regulation of PGC‐1α‐FoxO3 pathway.

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Oral Drugs Related with Muscle Wasting and Sarcopenia. A Review

Cited by 89 publications

References 85 publications

Incidence and Risk Factors for Frailty in the Community-Dwelling Elderly Population. A Two-Year Follow-Up Cohort Study

Incidence and Risk Factors for Frailty in the Community-Dwelling Elderly Population. A Two-Year Follow-Up Cohort Study

Factors Associated with Poor Muscle Mass and Strength in A Community-Dwelling Elderly Population: A Cross-Sectional Study

Beneficial effects of metformin on muscle atrophy induced by obesity in rats

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