Protein degradation in skeletal muscle during experimental hyperthyroidism in rats and the effect of beta-blocking agents.
beta-Blocking agents are increasingly used in the management of hyperthyroid patients. The effect of this treatment on increased muscle protein breakdown in the hyperthyroid state is not known. In the present study, experimental hyperthyroidism was induced in rats by daily ip injections of T3 (100 micrograms/100 g BW) during a 10-day period. Control animals received corresponding volumes of solvent. In groups of rats the selective beta-1-blocking agent metoprolol or the nonselective beta-blocker propranolol was infused by miniosmotic pumps implanted sc on the backs of the animals. Protein degradation was measured in incubated intact soleus and extensor digitorum longus muscles by determining tyrosine release into the incubation medium. The protein degradation rate in incubated extensor digitorum longus and soleus muscles was increased by 50-60% during T3 treatment. Metoprolol or propranolol did not influence muscle protein breakdown in either T3-treated or control animals. The results suggest that T3-induced increased muscle proteolysis is not mediated by beta-receptors, and muscle weakness and wasting in hyperthyroidism might not be affected by beta-blockers.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001835:Body Weight; D004435:Eating; D006980:Hyperthyroidism / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D008790:Metoprolol / Q000097:blood / Q000494:pharmacology; D009124:Muscle Proteins / Q000378:metabolism*; D009132:Muscles / Q000187:drug effects / Q000378:metabolism*; D011433:Propranolol / Q000097:blood / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D014284:Triiodothyronine / Q000097:blood
D000319:Adrenergic beta-Antagonists; D009124:Muscle Proteins; D014284:Triiodothyronine; D011433:Propranolol; D008790:Metoprolol