Download Synthesis of Thyroid Hormones

Synthesis of Thyroid Hormones
Unlike most endocrine glands, the thyroid gland stores large amounts of
some of the hormones it synthesizes. Thyroglobulin is produced and
secreted by follicle cells into the lumen of follicles as a colloid. There it
undergoes post-translational modification to produce functioning
thyroid hormones. Iodide molecules are added to the thyroglobulin
precursor to produce the hormones thyroxine and triiodothyronine.
Thyroxine is also known as T4 because it contains four atoms of iodine,
and triiodothyronine is also known as T3 because it contains three atoms
of iodine. In developed countries, the iodide required for hormone
synthesis is obtained primarily from iodized salt. However, seafood and
plants grown in iodine rich soil at lower elevations also provide the
required iodide. Since iodine as a molecule is quite volatile, the food
grown in higher elevations (lower atmospheric pressure) lacks sufficient
iodine. Iodide ions are actively transported into the follicular lumen
from the capillaries by follicle cells. Follicle cells are stimulated to
release stored T3and T4 from the lumen into the blood capillaries by
thyroid stimulating hormone (TSH), which is produced by the anterior
pituitary. Follicle cells also begin synthesizing more T3 and T4 in
response to TSH stimulation.
A third hormone, calcitonin, is produced by parafollicular cells, or C
cells of the thyroid. Calcitonin release is not controlled by TSH, but
instead is released when calcium ion concentrations in the blood rise.
Calcium ions bind to specific receptor on the C cell and stimulate release
of calcitonin. Calcitonin acts primarily in children to lower blood
calcium levels when levels get too high. Calcitonin causes decreased
tubular reabsorption of Ca2+ in the kidneys, leading to calcium loss in
urine. It inhibits bone resorption activity of osteoclasts and calcium
absorption in intestine to also reduce plasma calcium levels. It is also
suspected to have an indirect effect stimulating osteoblast activity and
development. However, in adult humans it appears to play only a minor
role in calcium homeostasis because abnormalities in calcitonin
production do not appear to be associated with specific plasma calcium
imbalances. Research has implicated its role during times of high
calcium demands, such as pregnancy and lactation.