Biological Significance of a Peculiar Pattern of Hormone Release from Iodine Deficient Rat Goitres

Abstract

THYROTROPIC pituitary hormone (TSH) is the principal regulator of thyroid activity. Besides promoting thyroid growth, TSH enhances iodide trapping as well as the release of iodinated compounds. The large intrathyroid iodine stores ultimately result from the net balance of TSH action on these processes. Of course, there must be a critical level of iodine supply to the thyroid gland for which increased trapping cannot compensate any longer. At this point, the thyroidal iodine stores will start to decrease. Work described here suggests that as soon as iodine depletion occurs, metabolism in the thyroid is profoundly changed in such a way as to provide the goitrous gland with an increasingly potent mechanism for triggering additional TSH release. Indeed, as a response to a decreasing iodide supply, the iodine deficient goitre curtails its hormone release much more efficiently than the normal thyroid. By this means the goitrous thyroid not only produces stronger stimuli for extra TSH secretion whenever a further decrease in iodine supply threatens to override the pre-established steady state, but in addition, the principal effects of TSH on thyroid function are no longer balanced. Our results indicate that trapping becomes heavily favoured over release. Thus excellent conditions are created for more efficient preservation of thyroidal iodine stores.