Effect of clenbuterol on skeletal muscle atrophy in mice induced by the glucocorticoid dexamethasone

Agbenyega, E.T.; Wareham, Anthony C.

doi:10.1016/0300-9629(92)90026-m

Cited by 41 publications

(27 citation statements)

References 35 publications

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“…46,47 These compounds were shown to be protective of muscle mass and function in animal models of denervation, sepsis, and corticosteroid atrophy, as well as in animal models of muscular dystrophy. [48][49][50][51] Similar results were obtained in studies of normal human volunteers, demonstrating the anabolic effects of the ␤2 agonists. 52 Based on this evidence, we undertook a pilot, 3-month, open-label trial of a sustained-release albuterol in FSHD, which then led to a 1-year, randomized, placebo-controlled trial.…”

supporting

confidence: 74%

Facioscapulohumeral Muscular Dystrophy

Tawil

Silvere

2011

Encyclopedia of Life Sciences

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Facioscapulohumeral muscular dystrophy (FSHD) is a common, dominantly inherited, muscle disease with a distinctive clinical presentation and a wide spectrum of disease severity. In greater than 95% of individuals with FSHD, the genetic defect is a loss of a critical number of D4Z4 macrosatellite repeats on chromosome 4q35. However, D4Z4 contractions are only pathogenic on specific, permissive chromosomal backgrounds. Recent evidence demonstrates that this permissive background facilitates the stable transcription of DUX4 , a retrogene sequence within D4Z4 that codes for a double homeodomain protein of unknown function. These findings implicate DUX4 in the pathophysiology of FSHD and for the first time, offer a target for therapeutic development in FSHD. Key Concepts: Epigenetic modifications can lead to gene derepression. FSHD results from reactivation of a retrogene.

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confidence: 74%

Facioscapulohumeral Muscular Dystrophy

Tawil

Silvere

2011

Encyclopedia of Life Sciences

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“…Notably, myostatin does not exert its action through NF-κB (25). β2-adrenergic agonists are potent muscle growth promoters in many animal species (26,27), resulting in skeletal muscle hypertrophy (28)(29)(30)(31). Formoterol is one of these compounds with important anti-cachectic effects in animal models.…”

Section: Introductionmentioning

confidence: 99%

Formoterol treatment downregulates the myostatin system in skeletal muscle of cachectic tumour-bearing rats

et al. 2011

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Abstract. Cachexia is a common systemic manifestation. Additionally, myostatin is known to be a negative regulator of skeletal muscle development. The present study aimed to investigate whether formoterol down-regulates the myostatin system in skeletal muscle of tumour-bearing rats. Real-time PCR and Western blotting were used for the analysis. Results showed that rats bearing the Yoshida AH-130 ascites hepatoma, a cachexia-inducing tumour, exhibited marked muscle wasting that affected the mass of the muscles studied. The cachectic animals exhibited a significant increase in the mRNA levels of the myostatin receptor (ActIIB) in gastrocnemius muscles. Notably, the expression of the various forms of follistatin, a protein with the opposite effects to those of myostatin, was significantly reduced as a result of the implantation of the tumour. When the animals were treated with formoterol, a β-agonist with anti-cachectic potential, increases in skeletal muscle weights were observed. The β-agonist significantly increased levels of various follistatin isoforms and significantly decreased the expression levels of the myostatin receptor. In addition, formoterol treatment resulted in a significant decrease of the myostatin protein content of the gastrocnemius muscle. In conclusion, the results presented indicate that certain anabolic actions of formoterol on the skeletal muscle of cachectic animals may be mediated via the myostatin system.

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“…Treatment with β 2 -adrenergic agonists results in skeletal muscle hypertrophy (11)(12)(13)(14), while they cause a reduction in the body fat content (15,16). Formoterol, one of these compounds, is a highly potent β 2 -adrenoceptor-selective agonist which combines the clinical advantages of rapid onset of action with duration of action.…”

Section: Introductionmentioning

confidence: 99%

Formoterol and cancer muscle wasting in rats: Effects on muscle force and total physical activity

Busquets

Toledo

Sirisi

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. Cancer cachexia occurs in the majority of cancer patients before death, and it is responsible for the death of 22% of cancer patients. One of the most relevant characteristics of cachexia is that of asthenia, which reflects significant muscle wasting noted in cachectic cancer patients The aim of the present study was to assess whether the β 2 -adrenergic agonist formoterol is associated with an improvement in physiological parameters such as grip force and total physical activity in cachetic rats. Administration of the β 2 -agonist formoterol (0.3 mg/kg for 7 days) in rats bearing Yoshida AH-130 ascites hepatoma tumors, a model which induces a strong loss of both body and muscle weight, resulted in a significant reversal of the muscle wasting process, as reflected by individual muscle weights. The anti-wasting effects of the drug were also observed in terms of total physical activity and grip force, thus resulting in an improvement in physical performance in cachectic tumor-bearing rats.

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Effect of clenbuterol on skeletal muscle atrophy in mice induced by the glucocorticoid dexamethasone

Cited by 41 publications

References 35 publications

Facioscapulohumeral Muscular Dystrophy

Facioscapulohumeral Muscular Dystrophy

Formoterol treatment downregulates the myostatin system in skeletal muscle of cachectic tumour-bearing rats

Formoterol and cancer muscle wasting in rats: Effects on muscle force and total physical activity

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