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Thyroid hormones act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth (synergy with growth hormone) and neural maturation, and increase the body's sensitivity to catecholamines (such as adrenaline) by permissiveness. [12]
Thyroid follicular cells (also called thyroid epithelial cells or thyrocytes [1]) are the major cell type in the thyroid gland, and are responsible for the production and secretion of the thyroid hormones thyroxine (T 4) and triiodothyronine (T 3).
Thyroxine, also known as T 4, is a hormone produced by the thyroid gland. It is the primary form of thyroid hormone found in the blood and acts as a prohormone of the more active thyroid hormone, triiodothyronine (T 3 ). [ 1 ]
David Marine in 1907 proved that iodine is necessary for thyroid function. [92] [91] Graves' disease was described by Robert James Graves in 1834. The role of the thyroid gland in metabolism was demonstrated in 1895 by Adolf Magnus-Levy. [97] Thyroxine was first isolated in 1914 and synthesized in 1927, and triiodothyroxine in 1952.
View/Edit Human View/Edit Mouse The thyrotropin receptor (or TSH receptor ) is a receptor (and associated protein) that responds to thyroid-stimulating hormone (also known as "thyrotropin") and stimulates the production of thyroxine (T4) and triiodothyronine (T3).
The pituitary gland secretes thyrotropin (TSH; Thyroid Stimulating Hormone) that stimulates the thyroid to secrete thyroxine (T4) and, to a lesser degree, triiodothyronine (T3). The major portion of T3, however, is produced in peripheral organs, e.g. liver, adipose tissue, glia and skeletal muscle by deiodination from
Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T 4), and then triiodothyronine (T 3) which stimulates the metabolism of almost every tissue in the body. [1]
Besides its increased function in producing extrathyroid T 3 in patients with hyperthyroidism, its function is less well understood than D2 or D3 [2] [7] Deiodinase 2, located in the ER membrane, converts T 4 into T 3 and is a major source of the cytoplasmic T 3 pool. [2] Deiodinase 3 prevents T 4 activation and inactivates T 3. [9]