Thyroid hormone autoregulation

The obvious consequence of mild-to-moderate iodine deficiency in a population is a high rate of goiter and thyroid multinodularity that will increase with age (Knudsen et ai, 2000a). The most important factor behind this development is probably not insufficient thyroid hormone production caused by iocfine deficiency, but autoregulation of thyroid iocfide utifization (Laurberg, 2000). 

Thyroid hormone synthesis as pg/rat increased 10-20 times to acute excess iodide (Fig.3) and 2-4 times to chronic excess iodide Thyroid hormone concentrations expressed as FBI or iodothyronines were constant regardless of iodide dose, and the degradation rates of thyroxine were not affected by excess iodide. Indeed, increase of organic iodine formation is far more than the increase of thyroidal organic iodine content To release the excessively organified iodine in the form of iodide from the thyroids is another good example of autoregulation by iodide. 

In normal human thyroids, there is no evidence that thyroidal iodine uptake is actually decreased by excess iodide and normal serum thyroid hormone concentrations and normal size of thyroid glands with normal serum TSH levels in spite of the greatly variable intake of dietary iodide is believed to be a good example of autoregulation of iodide. 

In contrast our normal IC of 380 ig/g agreed well with a maximal radioiodine uptake of 47% and the low mean dietary iodine of 46 ig daily (25). The lack of correlation between the IC and the thyroid function parameters is explained by the more efficient iodine utilization by the normal gland even under iodine deficiency (43). Normal responsiveness of TSH to TRH indicates, that an equilibrated hormone status may be maintained by means of thyroid autoregulation (63). 

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