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months supply of hormone. The amount of iodine contained in a normal gland, subject to an adequate iodine intake, is about 7-10mg. Release of hormone from the follicle is stimulated by TSH and inhibited by iodide and lithium.

Tg is a large protein (660kd) that serves as the matrix for thyroid hormone synthesis in the follicles and also as the storage vehicle. Tg synthesis is stimulated by TSH via the cyclic AMP mechanism. Of the 134 tyrosine residues in the molecule, no more than 15-17 are usually iodinated, including no more than 2-4 molecules of T4 and T3. The release of the hormone seems to result in the destruction of the Tg molecule, seemingly an inefficient process when the energy costs of synthesizing such a large molecule are considered. Normally, Tg is largely retained within the follicles, but it may be released into the blood stream in disease states. Tg is often produced by neoplasms derived from follicular cells and is a useful marker for recurrence of tumor.

Production of thyroid hormone is regulated by the pituitary gland through the secretion of TSH, which in turn is regulated by hypothalamic production of

Figure 2. A schematic representation of iodine metabolism in the thyroid gland. SCN-thiocyanate; ClO4-perchlorate; PTU-propylthiouracil; MT-methimazole; MIT&DIT-mono- and di-iodo-tyrosine; Tg-thyroglobulin; *-sites stimulated by TSH.

thyrotropin-releasing hormone (TRH). TRH is a tripeptide that may be transported to the pituitary along direct neuronal interconnections. Circulating levels of thyroid hormone, especially T3, provide the negative feedback required to regulate the level of TRH and TSH.

Circulating thyroid hormone is protein-bound. Thyroxine-binding proteins are present in the fetal blood stream by mid-gestation, an important consideration in Nuclear Medicine as maternal exposure to iodine isotopes will be associated with fetal uptake and retention through this mechanism.

Calcitonin, the secretory product of the C cells, is a polypeptide of 32 amino acids, whose major effect is to inhibit osteoclastic bone resorption. In humans the physiological importance of calcitonin remains unclear. Thyroidectomized patients with normal parathyroid gland function do not exhibit any apparent abnormality of bone metabolism.

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