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Thyroid-stimulating hormone (TSH) is a glycoprotein hormone produced by the anterior pituitary gland, primarily responsible for regulating the production and release of thyroid hormones thyroxine (T4) and triiodothyronine (T3) by stimulating the TSH receptor (TSHR) on thyroid follicular cells. It consists of two non-covalently linked subunits, alpha and beta, where the alpha subunit is common to similar hormones and the beta subunit confers specificity. Release of TSH is stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus, and inhibited by circulating thyroid hormones via a negative feedback loop. TSH levels serve as a sensitive clinical biomarker of thyroid axis integrity and are involved in disease states including hypothyroidism, hyperthyroidism, and autoimmune thyroid disorders such as Graves’ disease. TSH is itself not a receptor but acts via a specific G protein-coupled receptor (TSHR), making it an important target for therapies affecting thyroid function.
Drugs may increase (hormone replacement) or decrease (antithyroid agents) circulating T4/T3, thus changing feedback on TSH secretion. Antithyroid drugs reduce thyroid hormone synthesis, increasing TSH through feedback. Hormone replacement lowers TSH by restoring negative feedback.
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