Multiple actions of <i>β</i>-adrenergic agonists on skeletal muscle and adipose tissue

Yang, Yi Tien; McElligott, Mary Ann

doi:10.1042/bj2610001

Cited by 274 publications

(186 citation statements)

References 94 publications

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“…From these data, we conclude that the loss of Mstn function increased muscularity and decreased adiposity as expected. Clenbuterol treatment, similar to several other bAA, improves feed efficiency, increases protein accretion, and therefore muscle mass, and decreases fat mass (Ricks et al, 1984, Yang andMcElligott, 1989;Mersmann, 1998;Beermann, 2002). As a selective b-2 agonist (Hinkle et al, 2002), clenbuterol likely alters protein degradation (Reeds et al, 1986;Yimlamai et al, 2005) to increase protein accretion, but may also alter protein synthetic rates.…”

Section: Discussionmentioning

confidence: 99%

“…The use of b-adrenergic agonists (bAA) to increase muscle mass and decrease fat mass in several species is well established (Ricks et al, 1984;Mersmann, 1998;Beermann, 2002). Clenbuterol, although not approved for commercial use in livestock, increases muscle growth in mice and other species (Yang and McElligott, 1989). Another strategy to alter animal growth is to introduce mutations into the Mstn gene as occurs naturally in double-muscled cattle.…”

Section: Introductionmentioning

confidence: 99%

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The myostatin null mutation and clenbuterol administration elicit additive effects in mice

Dilger

Gabriel

Kutzler

et al. 2010

Animal

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In mice, the myostatin (Mstn) null mutation and treatment with clenbuterol both increase muscle growth and decrease fat mass. Our objective was to determine whether mechanistic overlap exists by administering clenbuterol to Mstn null mice. Male Mstn null and wild-type mice of similar genetic backgrounds received either 0 (control) or 20 p.p.m. clenbuterol in tap water free choice for 14 days. Several traits were measured to estimate muscle and fat growth. The Mstn null mutation resulted in increased body and empty carcass weight, increased muscle weights and decreased fat pad weights. Fat content was reduced and protein content was increased in the empty carcasses of Mstn null mice. Similarly, treatment with clenbuterol resulted in increased body and empty carcass weight, increased muscle weights and reduced fat pad weights. Fat content of empty carcasses and viscera was reduced and protein content of empty carcasses was increased with clenbuterol treatment. A significant interaction of genotype and clenbuterol treatment would indicate an altered responsiveness of Mstn null mice to clenbuterol. However, only the weight of gastrocnemius muscles exhibited a significant (P 5 0.01) interaction of genotype and clenbuterol treatment, indicating that Mstn null mice were less responsive to clenbuterol compared with wild-type mice. Thus, for all other traits, the impact of Mstn null mutation and clenbuterol treatment was completely additive. These data suggest that disruption of Mstn function does not alter the response of mice to b-adrenergic agonists.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The myostatin null mutation and clenbuterol administration elicit additive effects in mice

Dilger

Gabriel

Kutzler

et al. 2010

Animal

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“…For absolute power output, only the EDL muscles of mdx mice showed a difference following treatment, with the power output of treated mice being 118% that of the untreated mice. A '3 day on-3 day off' cycle was employed for weeks 2-20 in order to reduce attenuation of the clenbuterol response (Yang & McElligott, 1989). The clenbuterol solution was freshly prepared each week to avoid oxidation and possible reduction in its efficacy.…”

Section: Animal Groups and Drug Administrationmentioning

confidence: 99%

Power output of fast and slow skeletal muscles of mdx (dystrophic) and control mice after clenbuterol treatment

Lynch¹,

Hinkle²

2000

Exp. Physiol.

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“…β2-adrenergic agonists are potent muscle growth promoters in many animal species 8,9 , resulting in skeletal muscle hypertrophy [10][11][12][13] , while they cause a reduction of the body fat content 14,15 . These compositional alterations are associated with a redistribution of energy substrates, which are mobilized from storage sites for utilization by tissues such as muscle and brown adipose tissue 14 .…”

Section: Introductionmentioning

confidence: 99%

“…These compositional alterations are associated with a redistribution of energy substrates, which are mobilized from storage sites for utilization by tissues such as muscle and brown adipose tissue 14 . The intimate mechanisms by which these compounds exert such effects at the cellular level are still uncertain 9,14,15 , although changes in protein turnover are clearly involved 16 . The large number of physiological functions controlled by β-adrenergic receptors suggests that the mechanism(s) for the observed changes in carcass composition may be extremely complex.…”

Section: Introductionmentioning

confidence: 99%

Formoterol May Activate Rat Muscle Regeneration During Cancer Cachexia

Ametller¹,

Busquets²,

Fuster³

et al. 2011

Insciences J.

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PURPOSE: The development of cancer cachexia is the most common manifestation of advanced malignant disease. METHOD: The effects on muscle regeneration of β2-adrenoceptor agonist formoterol (0.3 mg/kg) were tested in cachectic tumour-bearing rats (Yoshida AH-130 ascites hepatoma). RESULTS: Administration of formoterol results in a significant increase in the mass and protein content of tibialis muscle in tumour-bearing-rats. This increase is associated with a decreased myogenin mRNA content together with an increased Pax-7 gene expression. Bupivacaine treatment by local injection results in an important reduction in tibialis weight together with significant increases in Pax-7, myogenin and MyoD gene expression. Formoterol treatment in bupivacaine-treated rats results in significant increases in Pax-7 together with significant decreases in myogenin mRNA content, suggesting that this β2-agonist is favouring muscle regeneration by stimulating the proliferation of satellite cells. Altogether, the data reinforce the potential role of formoterol in the treatment of muscle wasting diseases.

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Multiple actions of β-adrenergic agonists on skeletal muscle and adipose tissue

Cited by 274 publications

References 94 publications

The myostatin null mutation and clenbuterol administration elicit additive effects in mice

The myostatin null mutation and clenbuterol administration elicit additive effects in mice

Power output of fast and slow skeletal muscles of mdx (dystrophic) and control mice after clenbuterol treatment

Formoterol May Activate Rat Muscle Regeneration During Cancer Cachexia

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