Hormone synthesis and secretion

Lithium is associated with hypothyroidism in up to 34% of patients, and hypothyroidism may occur after years of therapy. Lithium appears to inhibit thyroid hormone synthesis and secretion. Patients with underlying autoimmune thyroiditis are more likely to develop lithium-induced hypothyroidism. Patients may require LT4 replacement even if lithium is discontinued. 

Mecfianism of Action Afat-soluble vitamin that is essential for absorption, utilization of calcium phosphafe, and normal calcification of bone. Therapeutic Effect Stimulates calcium and phosphate absorption from small inf esf ine, promof es secretion of calcium from bone fo blood, promofes renal tubule phosphate resorption, acts on bone cells to stimulate skeletal growth and on parathyroid gland to suppress hormone synthesis and secretion. 

Pituitary hormone stimulation of steroid hormone synthesis and secretion. 

Control of hormone synthesis and secretion in the anterior pituitary. Neurosecretory neurons in the hypothalamus liberate polypeptides that either stimulate or inhibit hormone synthesis by specialized pituitary cells containing the appropriate receptors. For example, GnRH stimulates gonadotroph cells in the pituitary to synthesize and secrete LH and FSH. These pituitary hormones then impinge on target cells, typically stimulating them to make other low-molecular-weight hormones. The end products of these cascades feedback-inhibit hormone production at either or both hypothalamic and pituitary levels. 

The thyroid gland is made up of multiple follicles that consist of a single layer of epithelial cells surrounding a lumen filled with colloid (thyroglobulin), the storage form of thyroid hormone. A diagram of the steps in thyroid hormone synthesis and secretion is shown in Figure 25.6. 

TABLE 73—1. Thyroid Hormone Synthesis and Secretion Inhibitors... 

Graves disease An autoimmune disorder in which antibodies overstimulate the production of thyroid hormones leading to a condition of hyperthyroidism, or elevated thyroid hormone synthesis and secretion. 

Growth hormone (somatotropin) is a polypeptide synthesized and secreted by somatotrophs in the anterior pituitary. Growth hormone synthesis and secretion is stimulated by the hypothalamic peptide growth hormone-... 

Thyrotropin-releasing factor (TRF) is produced in the hypothalamus and arrives at the pituitary via the hypophyseal portal blood system. TRF mediates the release of thyrotropin from the anterior hypophysis. The thyrotropin release is inhibited by thyroxine, presumably free thyroxine, and the inhibition is dose dependent. Thus excessive levels of thyroxine depress thyrotropin release, and lower thyroxine levels result in increased thyrotropin release from the anterior pituitary. TSH, in turn, stimulates thyroid hormone synthesis and secretion by the thyroid gland. Thyroxine and triiodothyronine are bound to specific binding proteins in the blood. The amounts and binding constants of the specific thyroid-binding proteins, together with the rate of thyroid hormone release from the thyroid, determine the amount of free thyroxine in the blood. Free thyroxine levels are determined not only by the rate of... 

Hormone synthesis and secretion are ultimately controlled by the central nervous system. Neurons in the hypothalamus either stimulate or inhibit hormone synthesis and/or secretion in the pituitary. Pituitary hormones initiate metabolic activities in their target cells. 

The first measurable effect of TSH on thyroid hormone metabolism is increased secretion, which is detectable within minutes. AU phases of hormone synthesis and secretion are eventually stimulated iodide uptake and organification, endocytosis, and proteolysis of thyroglobulin. There also is increased vascularity of the gland and hypertrophy and hyperplasia of thyroid cells. 

Iodide interferes with the TSH system as the fimit-ing factor in thyroid hormone synthesis. In iodine deficiency, low thyroid hormone synthesis and secretion lead to increased TSH secretion and thyroid stimulation. 

The mechanism leading to more hypothyroidism with higher iodine intake has not been fully elucidated. A high iodine load to the thyroid leads to inhibition of many thyroidal processes involved in hormone synthesis and secretion. Normally the thyroid will escape from this inhibition via downregulation of NIS and a subsequent fall in thyroidal iodide uptake (Eng et al., 1999). Apparently, this escape process is not fuUy effective in many people, especially people with a partly defective function of the thyroid because of thyroid autoimmunity or previous thyroid disease. 

A variety of internal (e.g., blood glucose level for insulin and glucagon) or external (e.g., stress for catecholamines) stimuli trigger hormone synthesis and secretion. Hormones have a basal secretion rate. This basal secretion is necessary for the maintenance of receptors in the target cell and to keep the tissue primed for hormones. 

Similar principles may be used for the assay of many other hormones. The radioimmunoassay technique is widely used in research into the mechanism of hormone synthesis and secretion, and is also used to determine the concentration of hormones in plasma in normal and pathogenic conditions. 

Ermans A.M., Dumont J.E., Bastenie P.A. 1963. Thyroid function in an endemic goiter. I. Impairment of hormones synthesis and secretion in the groitrous gland. II. Non-hormonal iodine escape from the goitrous gland. J.Clin.Endocrinol. Metab. 23 539-560. 

A. M.Ermans, J.E. Dumont, and P.A. Bastenie, Thyroid function in a goiter endemic I. Impairment of hormone synthesis and secretion in the goitrous gland. / CJin. Endoainal Metab. 23 539 (1963)... 

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