Metabolism and Excretion

Once iodine is 'captured' by the thyroid and thyroid hormones formed in the lumen of the follicles, stimulation of the gland causes release of the hormones into the circulation for uptake by peripheral tissues. Both production and release of the hormones are regulated in two ways. Stimulation is hormonally controlled by the hypothalamus of the brain through thyroid releasing hormone (TRH) which stimulates the pituitary gland to secrete thyroid stimulating hormone (TSH), which in turn stimulates the thyroid to release T3 and T4. In addition to the regulation of thyroid hormones by TSH, iodine itself plays a major role in autoregulation. The rate of uptake of iodine into the follicle, the ratio of T3 to T4, and the release of these into the circulation, among other things, are affected by the concentration of iodine in the gland. Thus, an increase in iodine intake causes a decrease in organification of iodine in the follicles and does not necessarily result in a corresponding increase in hormone release. Recent research suggests that this autoregulation is not entirely independent of TSH activity and that several other factors may contribute. However, regardless of the mechanism, these regulatory mechanisms allow for stability in hormone secretion in spite of wide variations in iodine intake.

When stimulated to release thyroid hormones, thyroglobulin is degraded through the activity of lysosomes and T3 and T4 are released and rapidly enter the circulation. Iodide freed in this reaction is for the most part recycled and the iodinated tyrosine reused for hormone production. Nearly all of the released hormones are rapidly bound to transport hormones, with 70% bound to thyroxine binding globulin (TBG). Other proteins, such as transthyre-tin (TTR), albumin, and lipoproteins, bind most of the remainder; with significant differences in the strengths of the affinity for the hormones, these proteins transport the hormones to different sites.

This remarkable ability of the thyroid to actively trap and store the iodine required creates a relatively steady state, with daily intake used to ensure full stores. T4, with a longer half-life, serves as a reservoir for conversion to the more active hormone, T3, with a much shorter half-life of 1 day. Target organs for thyroid hormone activity all play a role in the complex interplay between conversion of T4 to T3 deiodination, and metabolism of various other proteins involved with thyroid function. The liver,

In the follicle cells:

I- trapped from circulation and actively transported to lumen Thyroglobulin synthesized from amino acids and moves into lumen

Proteolysis releases T3 and T4 MIT and DIT are deiodinated T3 and T4 secreted Iodine is recycled

Figure 3 Thyroid follicle (courtesy of Kiely Houston).

In the follicle cells:

I- trapped from circulation and actively transported to lumen Thyroglobulin synthesized from amino acids and moves into lumen

Proteolysis releases T3 and T4 MIT and DIT are deiodinated T3 and T4 secreted Iodine is recycled which is estimated to contain 30% of the extrathy-roidal T4, is responsible, through the activity of the liver cell enzyme, deiodinase, for ensuring adequate supply of T3 to peripheral tissues and degradation of metabolic by-products. The kidney demonstrates a strong ability to take up the iodothyronines. Iodine is ultimately excreted in the urine, with average daily excretion rates of approximately 100 mg per day. This accounts for the vast majority of iodine excretion, with negligible amounts excreted in feces. Figure 3 illustrates a thyroid follicle and summarizes iodine transport.

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