Follicular thyroid hormone synthesis is regulated through the action of thyrotropin (thyroid stimulating hormone; TSH). Continued stimulation of thyroid by TSH results in immediate activation of follicular cell thyroid hormone synthesizing activity (follicular cells become columnar and luminal content of colloid is decreased). TSH interacts with follicular cell membrane receptors with resulting activation of adenylate cyclase and cAMP production.
All the subsequent follicular activities may be mediated through cAMP induced gene expression and activation of NIS, TG, peroxidase and proteins involved in iodine uptake and thyroid hormone synthesis.
In response to TSH, oxygen consumption is increased and glucose is taken up from medium and metabolized via pentose monophosphate shunt to generate NADPH. NADPH is required for reduction of molecular oxygen to hydrogen peroxide. the H2O2 is then used in oxidation of iodine to active form in the presence of thyroidal peroxidase.
As TG is secreted into follicular lumen, organification of iodine into tyrosine residues of TG may occur to yield 3 monoiodotyrosin (MIT) or 3,5-diiodotyrosine (DIT). Two DIT moieties couples to yield T4. Coupling of a MIT to a DIT yields T3.
On stimulation of thyroid by TSH, there is enhanced pinocytotic activity at apical follicular membrane. Thus, colloid is actively engulfed and carried to cell by endocytosis process. Active removal of colloid from lumen can be visualized as reabsorption lacunae.
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