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1 Medical Department M, Aarhus University Hospital, Aarhus, Denmark
2 Medical Department C, Aarhus University Hospital, Aarhus, Denmark
3 Department of Radiology R, Aarhus University Hospital, Aarhus, Denmark
4 Endocrine Research Unit, Mayo Clinic, Rochester, Minneapolis, USA
5 Medical Research Laboratories, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: anne.lene.riis{at}ki.au.dk.
Thyroid hormones have significant metabolic effects and muscle wasting and weakness are prominent clinical features of chronic hyperthyroidism. To assess the underlying mechanisms we examined seven hyperthyroid women with Graves disease before (Ht.) and after (Eut.) medical treatment and 7 control subjects (Ctr.). All subjects underwent a 3-h study in the post-absorptive state. After regional catheterization protein dynamics of the whole body and of the forearm muscles were measured by amino acid tracer dilution technique using 15N-phenylalanine and 2H4-tyrosine. Before treatment T3 was elevated (6.6 nmol/l) and whole body protein breakdown was 40% increased. The net forearm release of phenylalanine was increased in hyperthyroidism (µg/100ml/min): -7.0 ± 1.2 Ht. vs. -3.8 ± 0.8 Eut. (p = 0.04), -4.2 ± 0.3 Ctr. (p = 0.048). Muscle protein breakdown, assessed by phenylalanine rate of appearance was increased (µg/100ml/min): 15.5 ± 2.0 Ht. vs. 9.6 ± 1.4 Eut. (p = 0.03), 9.9 ± 0.6 Ctr. (p = 0.02). Muscle protein synthesis rate (Rd) did not differ significantly. Muscle mass and muscle function were 10-20% decreased before treatment. All abnormalities were normalized after therapy. In conclusion our results show that hyperthyroidism is associated with increased muscle amino acid release due to increased muscle protein breakdown. These abnormalities can explain the clinical manifestations of sarcopenia and myopathy.
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