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Research Article Free access | 10.1172/JCI109447

In Vitro and In Vivo Refractoriness to Thyrotropin Stimulation of Iodine Organification and Thyroid Hormone Secretion

James B. Field, Andrew Dekker, Gail Titus, Mary Eleanor Kerins, William Worden, and Rosalyn Frumess

Clinical Research Unit and Department of Medicine and Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

The Diabetes Research Laboratory of St. Luke's Hospital, Baylor College of Medicine, Houston, Texas 77025

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

Clinical Research Unit and Department of Medicine and Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

The Diabetes Research Laboratory of St. Luke's Hospital, Baylor College of Medicine, Houston, Texas 77025

Find articles by Dekker, A. in: PubMed | Google Scholar

Clinical Research Unit and Department of Medicine and Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

The Diabetes Research Laboratory of St. Luke's Hospital, Baylor College of Medicine, Houston, Texas 77025

Find articles by Titus, G. in: PubMed | Google Scholar

Clinical Research Unit and Department of Medicine and Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

The Diabetes Research Laboratory of St. Luke's Hospital, Baylor College of Medicine, Houston, Texas 77025

Find articles by Kerins, M. in: PubMed | Google Scholar

Clinical Research Unit and Department of Medicine and Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

The Diabetes Research Laboratory of St. Luke's Hospital, Baylor College of Medicine, Houston, Texas 77025

Find articles by Worden, W. in: PubMed | Google Scholar

Clinical Research Unit and Department of Medicine and Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

The Diabetes Research Laboratory of St. Luke's Hospital, Baylor College of Medicine, Houston, Texas 77025

Find articles by Frumess, R. in: PubMed | Google Scholar

Published July 1, 1979 - More info

Published in Volume 64, Issue 1 on July 1, 1979
J Clin Invest. 1979;64(1):265–271. https://doi.org/10.1172/JCI109447.
© 1979 The American Society for Clinical Investigation
Published July 1, 1979 - Version history
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Abstract

Earlier studies indicated that initial exposure of thyroid slices to thyrotropin diminished responsiveness of the adenylate cyclase-cyclic AMP system, glucose oxidation, and 32Pi incorporation into phospholipids upon readdition of the hormone. The present studies demonstrate that slices from dog, beef, and human thyroid glands initially incubated with thyrotropin (TSH) were less responsive to subsequent addition of the hormone when organification of iodide was examined. Increasing the amount of TSH did not overcome the refractoriness induced by the initial exposure to the hormone. Furthermore, the stimulatory effects of dibutyryl cyclic AMP and prostagladin E1 were abolished in slices previously incubated with TSH. Development of such refractoriness did not depend upon new protein synthesis and was not abolished by 1 mM prophylthiouracil in the first incubation. Addition of 0.1 μM thyroxine or triiodothyronine or 1.5 μM iodide during all three incubations did not modify the response to TSH, added for the first time in the third incubation. However, 1 mM iodide in the buffer during all three incubations inhibited the response to TSH during the third incubation. During the refractory period, effects of TSH on colloid droplet formation were also diminished. The in vivo effect of TSH on serum l- triiodothyronine in rats was significantly reduced when the rats had been injected with TSH 8 h earlier. These studies demonstrate that TSH-induced refractoriness also includes effects on organification of iodine and secretion of thyroid hormone. The results cannot be adequately explained by unresponsiveness of adenylate cyclase because effects of dibutyryl cyclic AMP and prostagladin E1 were also inhibited by prior exposure to TSH.

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