A STUDY OF THE MECHANISMS INVOLVED IN THE PRODUCTION OF IODINE-DEFICIENCY GOITER

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Abstract
An extensive study of the temporal sequence of changes in thyroid function after initiation of a low iodine regimen has been made in rats. Variables measured include: thyroid weight, I131 uptake, monoiodotyrosine/diiodotyrosine (MIT/DIT) and triiodothyronine/ thyroxine (T3/T4) ratios, iodide clearance, and I127 content. Also measured were protein-bound iodine (PBI), inorganic iodide and thyro-tropin (TSH) levels in the serum. Significant thyroid hypertrophy was produced during the 1st week and before there was a fall in serum PBI. Temporally related to the appearance of goiter were a rise in I131 uptake, MIT/DIT ratio and iodide clearance and a fall in thyroidal I127 concentration. In contrast, a fall in total thyroidal I127 appeared later and was closely correlated with a decline in serum PBI concentration and a rise in the thyroidal T3/T4 ratio. Manipulations such as hypo-physectomy, injections of iodide, thyroxine or TSH, and refeeding a high iodine diet gave results consistent with the view that changes produced by iodine deficiency involve both autonomous and TSH-dependent thyroidal mechanisms. Although elevated serum TSH levels could not be demonstrated until after the 1st week of the iodine-deficient regimen, the total evidence of these studies permits the conclusion that increased TSH secretion is the most important factor in producing the thyroidal response to iodine deficiency. It is shown that homeostatic mechanisms allow maintenance of a normal level of circulating thyroid hormone in an iodine-deficient state until the body iodine pool becomes too severly depleted to supply adequate iodide substrate to the thyroid. The changes observed closely resemble those found in human iodine-deficient goiters. Although the large goiters produced after several weeks of an iodine-deficient regimen were hyperplastic, they could readily be converted to typical colloid goiters by feeding a high iodine diet for a few days.