Reproduction   citetrack
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS  

Journal of Reproduction and Fertility (1972) 30 269-279
DOI: 10.1530/jrf.0.0300269
Copyright © 1972 Society for Reproduction and Fertility
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by LORSCHEIDER, F. L.
Right arrow Articles by REINEKE, E. P.
Right arrow Search for Related Content
PubMed
Right arrow Articles by LORSCHEIDER, F. L.
Right arrow Articles by REINEKE, E. P.

THYROID HORMONE SECRETION RATE IN THE LACTATING RAT

F. L. LORSCHEIDER and E. P. REINEKE

Summary.: Thyroid secretion rate (TSR) was determined in lactating and non-lactating rats by the thyroxine substitution and `direct output' methods. In lactating rats, apparent TSR as determined by the substitution method was significantly greater than that of controls when dietary iodine was deficient. By the direct output method, TSR was significantly reduced even when dietary iodine was adequate. It is concluded that the substitution method measures the physiological demand for thyroid hormone, which is greater during lactation, but represents true TSR only if iodine supplies are adequate. Results obtained by the direct output method show the actual TSR to be significantly reduced both during lactation and when dietary iodine is limited. Mean thyroid acinar cell height significantly increased as thyroidal iodine was depleted. It is concluded that, during lactation, TSH was elevated but iodine was insufficient to support the demand for thyroid hormone. The low serum T4 level observed in lactating rats, as determined by a competitive binding method, supports these conclusions.

Analysis of the methods of computation of TSR by direct output showed that (1) as thyroidal iodine supplies were depleted, thyroidal iodide accumulation became more efficient, (2) the iodine-deficient thyroid recycled a greater percentage of the available iodine, (3) thyroidal 131I uptake was reduced in lactating rats, (4) total thyroidal iodine was inversely correlated to its release rate (K4) from the thyroid, and (5) thyroidal iodine, and not K4, was the major factor influencing TSR under these experimental conditions.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS  
Copyright © 1972 by the Society for Reproduction and Fertility.