1955The Journal of Clinical Endocrinology & MetabolismRequires access

CONVERSION OF THYROXINE TO 3-5-3′-TRIIODOTHYRONINEIN VIVO*

Rosalind Pitt‐Rivers, John B. Stanbury, Betty Rapp

Open publisher page 96 citations

Abstract

THE principal iodinated compound of the blood is thyroxine (1, 2, 3). In addition, small amounts of triiodothyronine have been found in the blood of clinically euthyroid subjects and of patients with hyperthyroidism (4). Both thyroxine and triiodothyronine have been identified in the normal rat and ox thyroid gland (5). However, it has not been shown whether the triiodothyronine which is present in the peripheral blood is secreted directly by the thyroid gland, or whether it is derived from degradation of previously secreted thyroxine. The present study demonstrates that triiodothyronine can be formed in the human subject from thyroxine in the absence of the thyroid gland, and confirms in man the finding of Gross and Leblond (6) that “unknown 1” (later shown to be triiodothyronine) can be formed in certain peripheral tissues in the thyroidectomized animal. Six patients with typical athyreotic myxedema were chosen. The diagnosis in each case was proved by measurements of basal metabolic rate and of serum concentration of protein-bound iodine (0.0 to 1.3 μg. per 100 ml.). Five patients were then given thyroxine in doses varying from 50 to 300 micrograms daily.

About this research paper

What this paper is about

THE principal iodinated compound of the blood is thyroxine (1, 2, 3). In addition, small amounts of triiodothyronine have been found in the blood of clinically euthyroid subjects and of patients with hyperthyroidism (4). Both thyroxine and triiodothyronine have been identified in the normal rat and ox thyroid gland (5). However, it has not been shown whether the triiodothyronine which is present in the peripheral blood is secreted directly by the thyroid gland, or whether it is derived from degradation of previously secreted thyroxine. The present study demonstrates that triiodothyronine can be formed in the human subject from thyroxine in the absence of the thyroid gland, and confirms in man the finding of Gross and Leblond (6) that “unknown 1” (later shown to be triiodothyronine) can be formed in certain peripheral tissues in the thyroidectomized animal. Six patients with typical athyreotic myxedema were chosen. The diagnosis in each case was proved by measurements of basal metabolic rate and of serum concentration of protein-bound iodine (0.0 to 1.3 μg. per 100 ml.). Five patients were then given thyroxine in doses varying from 50 to 300 micrograms daily.

Why it matters

OpenAlex reports 96 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

THE principal iodinated compound of the blood is thyroxine (1, 2, 3). In addition, small amounts of triiodothyronine have been found in the blood of clinically euthyroid subjects and of patients with hyperthyroidism (4). Both thyroxine and triiodothyronine have been identified in the normal rat and ox thyroid gland (5). However, it has not been shown whether the triiodothyronine which is present in the peripheral blood is secreted directly by the thyroid gland, or whether it is derived from degradation of previously secreted thyroxine. The present study demonstrates that triiodothyronine can be formed in the human subject from thyroxine in the absence of the thyroid gland, and confirms in man the finding of Gross and Leblond (6) that “unknown 1” (later shown to be triiodothyronine) can be formed in certain peripheral tissues in the thyroidectomized animal. Six patients with typical athyreotic myxedema were chosen. The diagnosis in each case was proved by measurements of basal metabolic rate and of serum concentration of protein-bound iodine (0.0 to 1.3 μg. per 100 ml.). Five patients were then given thyroxine in doses varying from 50 to 300 micrograms daily.

Key concepts: Euthyroid, Triiodothyronine, Myxedema, Endocrinology, Internal medicine, Thyroid, Iodine, Reverse triiodothyronine

Related papers

Back to paper searchBrowse research topicsOriginal source
CONVERSION OF THYROXINE TO 3-5-3′-TRIIODOTHYRONINEIN VIVO* — Research Paper | ScholarLens