Homeostatic adjustments of iodine metabolism and tissue iodine to widely varying iodine supply in I-125 labeled rats

Thirty-two growing rats were fed restrictively (13 g/day) 10 semisynthetic diets which were adjusted to total iodine contents of 60, 90, 120, 150, 180 , 400, 800, 1600, 5000 and 20000 ng/g by adding potassium iodide. After 2 N ecks of collecting faecal and renal excretions the animals were killed and dissected completely into various tissues. True absorption of dietary iodin e averaged 99% of iodine intake irrespective of the level of iodine supply. Endogenous faecal excretion remained largely constant (about 0.2 mu g/day) . Urinary iodine rose iron 1 to 273 mu g/day with a tendency for a reduced excretion rate ac low iodine supply. Raising dietary iodine increased iodin e retention from negative values to a plateau of about 0.1 mu g/day which w as achieved at 150 ng/g of dietary iodine. Above 400 ng/g of dietary iodine the retention continued to increase up to 8 mu g/day at highest iodine int ake. Thyroidal iodine concentration rose from 42 to 81 mu g/g and turned in to a plateau at 150 ng/g of dietary iodine. The plateau was maintained up t o dietary iodine levels of about 1600 ng/g and then increased ru 222 mu g/g at highest iodine intake. The extrathyroidal tissues revealed comparably s mall changes in iodine concentration as long as dietary iodine content did nor exceed 400 ng/g whereas a further rise in iodine supply increased the r espective concentrations up ro factor 20 to 50 at highest iodine level. Ar low and medium iodine supply, the whole-body iodine was localized mainly in the thyroid gland (40%), skin (35%), hair (6%) and carcass (18%). At highe st iodine level, the contribution of thyroidal iodine dropped to 8% at favo ur especially of the skin. The contribution of other tissues was of minor q uantitative relevance. At. all levels of dietary iodine supply the injected I-125 activity was recovered completely in excrements and tissues indicati ng that there were no quantitatively relevant gaseous losses of iodine. In conclusion, the iodine metabolism is subject to homeostatic regulation. It starts to work at dietary iodine contents of 150 ng/g which denotes the min imum requirement of iodine. At dietary iodine contents of 800 ng/g and more the compensatory capacity of iodine homeostasis seems to be overcharged wi th the consequence of extensive iodine accumulations especially in extrathy roidal tissues.