help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chernausek, S. D.
Right arrow Articles by Van Wyk, J. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chernausek, S. D.
Right arrow Articles by Van Wyk, J. J.

Endocrinology, Vol 111, 1534-1538, Copyright © 1982 by Endocrine Society


ARTICLES

Influence of hypothyroidism on growth hormone binding by rat liver

SD Chernausek, LE Underwood and JJ Van Wyk

The binding of 125I-iodinated human GH ([125I]iodo-hGH) to crude, membrane-rich preparations from the livers of thyroidectomized male rats was examined to determine if alterations in GH binding might explain hypothyroid-induced growth failure. Membrane preparations from chronically hypothyroid rats bound nearly twice as much labeled hGH (12.8 +/- 2.5%; mean +/- 1 SD) as those from normal rats (6.6 +/- 1.4%) or thyroxine-treated thyroidectomized animals (7.0 +/- 1.1%). Binding by membrane preparations from hypothyroid rats treated with hGH for 2 weeks was 12.3%. By Scatchard analysis the apparent affinities of the membrane preparations for hGH were relatively constant (Ka = 2.30-2.88 X 10(9) M-1) among the experimental groups. Ovine PRL was only 1.4% as potent as hGH in displacing [125I]iodo-hGH from the liver preparations, indicating that hGH was bound primarily to somatogenic sites. Since administration of hGH did not reduce the binding of [125I]iodo-hGH, it is unlikely that the increase in hGH binding in hypothyroidism is mediated by a reduction in the ambient GH concentration. Furthermore, this increase in [125I]iodo-hGH binding indicates that an alteration in binding of GH to its receptor probably does not mediate either the low somatomedin levels or the growth failure that result from hypothyroidism.


This article has been cited by other articles:


Home page
J. Clin. Endocrinol. Metab.Home page
R. P. Peeters, A. W. van den Beld, H. van Toor, A. G. Uitterlinden, J. A. M. J. L. Janssen, S. W. J. Lamberts, and T. J. Visser
A Polymorphism in Type I Deiodinase Is Associated with Circulating Free Insulin-Like Growth Factor I Levels and Body Composition in Humans
J. Clin. Endocrinol. Metab., January 1, 2005; 90(1): 256 - 263.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
A. J. Forhead, J. Li, J. C. Saunders, M. J. Dauncey, R. S. Gilmour, and A. L. Fowden
Control of ovine hepatic growth hormone receptor and insulin-like growth factor I by thyroid hormones in utero
Am J Physiol Endocrinol Metab, June 1, 2000; 278(6): E1166 - E1174.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1982 by The Endocrine Society