Thyroid-stimulating hormone (TSH)
Also known as: TSH, thyrotropin, thyrotrophin
A glycoprotein from thyrotrophs that stimulates every step of thyroid hormone synthesis and release and the growth of the thyroid; serum TSH is the most sensitive single test of thyroid function.
Overview
TSH consists of an α-subunit shared with LH, FSH and hCG and a hormone-specific β-subunit. It binds the TSH receptor on the basolateral membrane of thyroid follicular cells, a GPCR coupled mainly to Gs (cAMP/PKA) and, at higher concentrations, to Gq (PLC). Acute effects include increased colloid endocytosis and hormone release within minutes; over hours to days it increases NIS, TPO and thyroglobulin expression, iodide uptake, blood flow, and causes follicular hypertrophy and hyperplasia (goitre when chronic).
Because TSH secretion is exquisitely sensitive to feedback by thyroid hormone (a log-linear relationship — a 2-fold change in free T4 produces roughly a 100-fold change in TSH), serum TSH detects thyroid dysfunction earlier than T4 itself, provided the pituitary is normal.
- Location
Source: thyrotrophs of the anterior pituitary. Target: thyroid follicular cells (TSH receptors also on orbital fibroblasts and adipocytes).
Function
- Stimulates iodide uptake, thyroglobulin iodination, coupling and T4/T3 release.
- Stimulates growth and vascularity of the thyroid.
- Physiology
Class: glycoprotein (α + β subunits, ≈28 kDa). Receptor: TSHR — Gs/cAMP (and Gq). Half-life ≈1 h. Secretion has a nocturnal peak.
- Regulation
Stimulated by TRH; inhibited by T4/T3 (via local pituitary T4→T3 conversion), somatostatin, dopamine and glucocorticoids.
Clinical significance
Interpreting TSH
High TSH + low T4 → primary hypothyroidism; high TSH + normal T4 → subclinical hypothyroidism. Low TSH + high T4/T3 → primary hyperthyroidism. Low/normal TSH + low T4 → secondary (central) hypothyroidism, where TSH is useless for monitoring therapy. Normal/high TSH + high T4 → TSH-oma or thyroid hormone resistance.
hCG cross-reactivity
hCG shares the α-subunit and weakly activates the TSH receptor, so TSH falls in the first trimester and high-hCG states (hyperemesis gravidarum, molar pregnancy) can cause gestational thyrotoxicosis.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.