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Research Article Free access | 10.1172/JCI112424

Interrelationships among thyroxine, growth hormone, and the sympathetic nervous system in the regulation of 5'-iodothyronine deiodinase in rat brown adipose tissue.

J E Silva and P R Larsen

Find articles by Silva, J. in: JCI | PubMed | Google Scholar

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Published April 1, 1986 - More info

Published in Volume 77, Issue 4 on April 1, 1986
J Clin Invest. 1986;77(4):1214–1223. https://doi.org/10.1172/JCI112424.
© 1986 The American Society for Clinical Investigation
Published April 1, 1986 - Version history
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Abstract

Thyroxine (T4) and reverse triiodothyronine are potent inhibitors of brown adipose T4 5'-deiodinase (BAT 5'D). This effect does not require protein synthesis and is due to an acceleration of the rate of disappearance of the enzyme. Growth hormone (GH) also inhibits BAT 5'D but by a mechanism mediated through a long-lived messenger that correlates with growth rate. This explains the failure of BAT 5'D to increase abruptly after thyroidectomy as does the type II 5'-deiodinase in pituitary and central nervous system or the BAT 5'D itself after hypophysectomy. Although virtually inactive when given acutely, triiodothyronine replacement partially reduces BAT 5'D in hypophysectomized and thyroidectomized (Tx) animals probably as a result of improvement of systemic hypothyroidism and an increase in GH levels in the Tx rats. The fine balance between these inhibitory factors and the stimulatory effects of the sympathetic nervous system suggests an important physiologic role for the enzyme in this tissue.

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