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Changes in Thyroidal Economy in Rats Bearing Transplantable Walker 256 Carcinomas^*

Division of Endocrinology and Metabolism, Department of Medicine, Montefiore Hospital and Medical Center, and the Albert Einstein College of Medicine Bronx, New York 10467

Address all correspondence and requests for reprints to: M. I. Surks, M.D., Montefiore Hospital and Medical Center, 111 East 210th Street, Bronx, New York 10467.

Abstract

Rats bearing transplanatable Walker 256 carcinomas have decreased hepatic nuclear T3 receptor concentration and decreased plasma concentrations of total and free T₄ and T₃. In the present studies, we investigated the mechanisms whereby plasma T₄ is decreased in tumor-bearing (T) rats. Mean plasma T₄ concentrations were significantly decreased in thyroidectomized T rats receiving daily treatment with T₄ (3 µg/100 g BW). When tumor size was 6.5 ± 0.8% of body weight, plasma T₄ was only 28% of control. This observation suggested alterations in the extrathyroidal metabolism of T₄ in T rats. Measurements of plasma T₄ binding and metabolism in groups of control (C) and T rats showed that the earliest change in thyroidal economy in rats with small neoplasms was a significant decrease in plasma T₄ binding, and this was associated with a significant and proportional increase in the T₄ MCR. With increasing tumor size, decreased plasma binding contributed to a smaller degree to the persistent elevation in the rate of T₄ metabolism. This finding suggested that cellular processes involved in T₄ metabolism were stimulated in T rats. Despite an increased rate of T₄ metabolism in T rats, T₄ turnover' (nanograms per 100 g BW/h) remained unchanged from C or was significantly decreased. This appeared to be due to the fact that plasma TSH in T rats was similar to that in C rats, and thyroidal activity, assessed by the thyroid to serum iodide concentration ratio, was decreased in T rats. Thus, the decrease in plasma T₄ in T rats appears to be due to a decrease in plasma T₄ binding, an increase in the rate of cellular T₄ metabolism, a failure of the hypothalamic-pituitary axis to augment TSH secretion in response to decreased plasma T₄ and T₃ concentrations, and a decrease in thyroidal activity based on either hyporesponsiveness to circulating TSH or secretion of abnormal TSH with decreased biological activity. (Endocrinology 106: 1386, 1980)

Footnotes

^* This work was supported by NIH Grants 1R01-CA-164363-04 and 1R01-CA-24604-01 and NIH Training Grant Am-07004-05 (to S.J.M.).

Received August 10, 1979.