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Thyroid Inhibition in the Rat: Comparison of Effects of Thyroid Hormone Treatment, Hypophysectomy and Anti-TSH Antibody

Seymour Reichlin, Rita L. Boshans

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Abstract

The thyroid gland inhibition which follows administration of excess thyroid hormone (TH) is a classic illustration of feedback control of pituitary thyrotropic hormone (TSH) secretion. Recent experiments demonstrating that thyroxine inhibits thyroidal iodide trapping and release rate more completely than does hypophysectomy suggest that there may be pituitary factors other than TSH which influence thyroid gland activity. This problem has been studied in rats by comparing the effects of thyroxine treatment with the effects of TSH deficiency induced in 2 different ways: by hypophysectomy, which gives, in addition, deficiency of other tropic hormones; and by treatment with anti-TSH antibody, which produces selective interference only with thyrotropic stimulation. In normal rats, the thyroidal 13lI release rate was reduced to the same degree by TH, by hypophysectomy and by anti-TSH. As measured by the distribution of iodinated amino acids in thyroid homogenates 24 hr after 131I injection, hormonogenesis was suppressed equally by hypophysectomy and by T4. These changes included a decline in the proportion of iodinated thyronines and a rise in the proportion of MIT relative to DIT. Neither anti-TSH nor TH lowered still further the already depressed thyroid function of hypophysectomized rats. Under the conditions of this experiment, no evidence was obtained that the thyroid gland inhibition produced by TH differed from that produced by removal of TSH influence on the thyroid gland by hypophysectomy or by anti-TSH. These findings support the classic view that thyroxine inhibits the thyroid gland by its effects in abolishing TSH stimulation. (Endocrinology75: 571, 1964)

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The thyroid gland inhibition which follows administration of excess thyroid hormone (TH) is a classic illustration of feedback control of pituitary thyrotropic hormone (TSH) secretion. Recent experiments demonstrating that thyroxine inhibits thyroidal iodide trapping and release rate more completely than does hypophysectomy suggest that there may be pituitary factors other than TSH which influence thyroid gland activity. This problem has been studied in rats by comparing the effects of thyroxine treatment with the effects of TSH deficiency induced in 2 different ways: by hypophysectomy, which gives, in addition, deficiency of other tropic hormones; and by treatment with anti-TSH antibody, which produces selective interference only with thyrotropic stimulation. In normal rats, the thyroidal 13lI release rate was reduced to the same degree by TH, by hypophysectomy and by anti-TSH. As measured by the distribution of iodinated amino acids in thyroid homogenates 24 hr after 131I injection, hormonogenesis was suppressed equally by hypophysectomy and by T4. These changes included a decline in the proportion of iodinated thyronines and a rise in the proportion of MIT relative to DIT. Neither anti-TSH nor TH lowered still further the already depressed thyroid function of hypophysectomized rats. Under the conditions of this experiment, no evidence was obtained that the thyroid gland inhibition produced by TH differed from that produced by removal of TSH influence on the thyroid gland by hypophysectomy or by anti-TSH. These findings support the classic view that thyroxine inhibits the thyroid gland by its effects in abolishing TSH stimulation. (Endocrinology75: 571, 1964)

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Available abstract

The thyroid gland inhibition which follows administration of excess thyroid hormone (TH) is a classic illustration of feedback control of pituitary thyrotropic hormone (TSH) secretion. Recent experiments demonstrating that thyroxine inhibits thyroidal iodide trapping and release rate more completely than does hypophysectomy suggest that there may be pituitary factors other than TSH which influence thyroid gland activity. This problem has been studied in rats by comparing the effects of thyroxine treatment with the effects of TSH deficiency induced in 2 different ways: by hypophysectomy, which gives, in addition, deficiency of other tropic hormones; and by treatment with anti-TSH antibody, which produces selective interference only with thyrotropic stimulation. In normal rats, the thyroidal 13lI release rate was reduced to the same degree by TH, by hypophysectomy and by anti-TSH. As measured by the distribution of iodinated amino acids in thyroid homogenates 24 hr after 131I injection, hormonogenesis was suppressed equally by hypophysectomy and by T4. These changes included a decline in the proportion of iodinated thyronines and a rise in the proportion of MIT relative to DIT. Neither anti-TSH nor TH lowered still further the already depressed thyroid function of hypophysectomized rats. Under the conditions of this experiment, no evidence was obtained that the thyroid gland inhibition produced by TH differed from that produced by removal of TSH influence on the thyroid gland by hypophysectomy or by anti-TSH. These findings support the classic view that thyroxine inhibits the thyroid gland by its effects in abolishing TSH stimulation. (Endocrinology75: 571, 1964)

Key concepts: Hypophysectomy, Internal medicine, Endocrinology, Thyroid, Hormone, Stimulation, Iodine, Pituitary gland

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