The Effect of Acute Iodide Depletion on Thyroid Function in Man.

In addition to a variety of effects on the intermediary metabolism of the thyroid gland, and perhaps as a consequence thereof, the thyrotropic hormone of the anterior pituitary (TSH) induces thyroidal hypertrophy, hyperplasia, and hypervascularity and stimulates most, if not all, phases of iodine metabolism leading to the synthesis and secretion of thyroid hormone (1, 2). Decreases in thyroid cell size, blood flow, and hormone synthesis occur in the absence of TSH stimulation. For the foregoing reasons, it is generally agreed that TSH is the major regulator of thyroid structure and function. Nevertheless, there is growing evidence that the thyroid gland contains mechanisms for modifying its own function. Thus, in hypophysectomized rats, dietary iodine restriction increases thyroid uptake of I' and may enhance mean acinar cell height (3, 4). Furthermore, in hypophysectomized rats given either no TSH or constant doses of this hormone, the activity of the thyroid iodide-transport mechanism varies inversely with the glandular content of organic iodine (5-10). The effects of such autoregulatory mechanisms in the absence of TSH are relatively small; their most important role probably stems from their ability to modify the glandular response to trophic stimulation (8-10). There are, apparently, no data as to whether similar autoregulatory phenomena occur in the human thyroid. In normal subjects, as much as 2 mg of iodide can be acutely administered without appreciably changing the percentage uptake