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However, low-dose clenbuterol treatment for 2 wk significantly reduced fasting blood glucose by 12. 9% in WT and 14. 8% in UCP1-/- mice. Clenbuterol treatment improved glucose and insulin tolerance in both genotypes compared with HFD controls and normalized to chow-fed control mice independent of body mass and composition alterations. When STZ-treated mice were co-injected i. PMID: 10065331 DOI: 10. Clenbuterol has been proposed for the treatment of muscle wasting disorders, but its long-term effects on skeletal muscle function have not been tested rigorously. Intracellular β2-adrenergic receptor signaling specificity in mouse skeletal muscle in response to single-dose β2-agonist clenbuterol treatment and acute exercise. In mice injected with IS, clenbuterol treatment increased the muscle mass and restored the tissue ROS level but failed to improve muscle weakness. Results: Propranolol-treated mice had decreased weight gain (p<0. 01), in comparison with clenbuterol-treated mice. Left ventricular mass was decreased (and comparable to wild-type) in ERT only and clenbuterol-treated groups of mice, and unchanged in propranolol-treated mice 
 

When STZ-treated mice were co-injected i. BCD- and BCD + clenbuterol–treated mice showed comparable levels of locomotor movements that significantly improved over time. Soleus muscle mass and soleus and extensor digitorum longus cross-sectional area significantly increased in both groups of BCD-treated mice, with greater effects in BCD + clenbuterol–treated animals. Results: Propranolol-treated mice had decreased weight gain (p<0. 01), in comparison with clenbuterol-treated mice. Left ventricular mass was decreased (and comparable to wild-type) in ERT only and clenbuterol-treated groups of mice, and unchanged in propranolol-treated mice. In normal mice clenbuterol, a β 2 -AR-specific agonist, considerably reduced Jo2-induced liver apoptosis and death; salbutamol, another β 2 -AR-selective agonist, also reduced Jo2-induced apoptosis and retarded death but with less efficacy than clenbuterol; and propranolol blocked the protective effect of clenbuterol. The purpose of this study was to determine the effects of chronic treatment with the beta 2 adrenergic receptor agonist clenbuterol on endothelial progenitor cells (EPC) in a well-characterized model of heart failure, the muscle LIM protein knockout (MLP(-/-)) mouse. In mice injected with IS, clenbuterol treatment increased the muscle mass and restored the tissue ROS level but failed to improve muscle weakness 
 
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