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Triiodothyronine (T3): The Active Thyroid Hormone—Production, Action, and Regulation

Triiodothyronine (T3) is the biologically active thyroid hormone. Though the thyroid secretes mostly thyroxine (T4), T3 exerts the majority of metabolic effects.

Production

  • Thyroidal (~20%): Direct secretion.
  • Peripheral conversion (~80%): T4 → T3 via deiodinases (D1 in liver/kidney; D2 in brain, pituitary, brown fat, muscle).
  • Reverse T3 (rT3): Inactive metabolite from T4 via D3; elevated in illness/starvation (non-thyroidal illness syndrome).

Transport & Bioavailability

  • Bound to thyroid-binding globulin (TBG), transthyretin (TTR), albumin.
  • Free T3 (fT3) (~0.3% of total) is the active fraction entering cells.

Mechanism of Action

  1. fT3 diffuses into target cells.
  2. Binds nuclear thyroid hormone receptors (TRα, TRβ) → modulates gene transcription.
  3. Regulates metabolic rate, thermogenesis, protein synthesis, lipid/carbohydrate metabolism, growth/development, cardiac output, CNS maturation.

Regulation: Hypothalamic-Pituitary-Thyroid Axis

  • Low T3/T4 → Hypothalamus releases TRH → Anterior pituitary releases TSH → Thyroid synthesizes/releases T4/T3.
  • High T3/T4 → Negative feedback inhibits TRH & TSH.
  • TSH is the most sensitive clinical marker of thyroid status.

Clinical Relevance

  • Hyperthyroidism: Elevated T3 (T3 toxicosis) or T4; suppressed TSH. Symptoms: tachycardia, weight loss, tremor, heat intolerance, anxiety.
  • Hypothyroidism: Low T3/T4; elevated TSH (primary). Symptoms: fatigue, cold intolerance, weight gain, bradycardia.
  • Non-thyroidal illness: Low T3, normal/low T4, normal/low TSH—adaptive, not true thyroid disease.
  • Medication effects: Amiodarone, beta-blockers, glucocorticoids inhibit D1/D2 → lower T3.

Free T3 measurement is useful in suspected T3 toxicosis, monitoring thyroid hormone replacement, and evaluating non-thyroidal illness.

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