TSH Initiation of Hormone Secretion by Rat Thyroid Lobesin Vitro
P. G. Malan, John Strang, Winton Tong
Abstract
P. G. Malan, John Strang, Winton Tong
Abstract
The actions of TSH to initiate the stimulation of thyroidal secretion were studied with thyroid lobes taken from 131I-injected rats. TSH treatment was limited to brief preincubations, following which the glands were washed with trypsin to remove and inactivate the TSH. Thereafter, the degree of stimulation ascertained by observing the release of 131-iodide, T3 and T4 by the glands during 2-hr test incubations, was compared with the maximal stimulation exhibited by glands incubated for 2 hr v/ith TSH present throughout. Preincubation for 10 min with TSH (0.2 U/ml) initiated a maximal stimulation of secretory activity that continued for 2 to 4 hr after removal of the TSH. Evidently the TSH activated initiating steps in the sequence of reactions comprising the secretory response. Once these steps were completed, the remaining reactions leading to the liberation of secretory products continued even in the absence of TSH. Since cyclic AMP levels in the thyroid lobes were promptly raised by TSH, and since the secretory response could be elicited by dibutyryl cyclic AMP, one of the initial reactions stimulated by TSH may well be the adenyl cyclase reaction. However, since tissue cyclic AMP levels decreased rapidly after withdrawal of the TSH, and since stimulated secretory activity continued thereafter at basal cyclic AMP levels, other initiating events must also have been activated. The present findings suggest that the principal event activated by TSH is the phagocytic uptake of colloid by the thyroid cells. In addition, the possibility remains that the intracellular mechanisms for the utilization of the resorbed colloid and the release of secretory products are also activated by TSH or cyclic AMP, but evidence for this is presently not at hand. (Endocrinology95: 397, 1974)
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The actions of TSH to initiate the stimulation of thyroidal secretion were studied with thyroid lobes taken from 131I-injected rats. TSH treatment was limited to brief preincubations, following which the glands were washed with trypsin to remove and inactivate the TSH. Thereafter, the degree of stimulation ascertained by observing the release of 131-iodide, T3 and T4 by the glands during 2-hr test incubations, was compared with the maximal stimulation exhibited by glands incubated for 2 hr v/ith TSH present throughout. Preincubation for 10 min with TSH (0.2 U/ml) initiated a maximal stimulation of secretory activity that continued for 2 to 4 hr after removal of the TSH. Evidently the TSH activated initiating steps in the sequence of reactions comprising the secretory response. Once these steps were completed, the remaining reactions leading to the liberation of secretory products continued even in the absence of TSH. Since cyclic AMP levels in the thyroid lobes were promptly raised by TSH, and since the secretory response could be elicited by dibutyryl cyclic AMP, one of the initial reactions stimulated by TSH may well be the adenyl cyclase reaction. However, since tissue cyclic AMP levels decreased rapidly after withdrawal of the TSH, and since stimulated secretory activity continued thereafter at basal cyclic AMP levels, other initiating events must also have been activated. The present findings suggest that the principal event activated by TSH is the phagocytic uptake of colloid by the thyroid cells. In addition, the possibility remains that the intracellular mechanisms for the utilization of the resorbed colloid and the release of secretory products are also activated by TSH or cyclic AMP, but evidence for this is presently not at hand. (Endocrinology95: 397, 1974)
Key concepts: Internal medicine, Endocrinology, Stimulation, Thyroid, Secretion, Hormone, Basal (medicine), Thyroid-stimulating hormone