The essential metabolic process where the primary thyroid hormone secreted by the gland, thyroxine (T4), is enzymatically deiodinated in peripheral tissues, primarily the liver and kidneys, to form the highly biologically active hormone, triiodothyronine (T3). This conversion is a crucial regulatory step, as T3 is the molecule that directly interacts with nuclear receptors to modulate gene expression and metabolic rate. Impaired conversion is a common cause of hypothyroid symptoms.
Origin
This is a fundamental concept in thyroid physiology and clinical endocrinology, describing the peripheral activation of the prohormone T4 into the active hormone T3. The process is governed by a family of deiodinase enzymes. Clinical focus on this conversion is vital for understanding non-thyroidal illness and peripheral hormone resistance.
Mechanism
The conversion is catalyzed by deiodinase enzymes (D1, D2, and D3). Specifically, Type 1 (D1) and Type 2 (D2) deiodinases remove an iodine atom from the outer ring of T4 to produce T3, effectively activating the hormone. Conversely, Type 3 (D3) deiodinase converts T4 into inactive reverse T3 (rT3), acting as a metabolic brake. The balance of these enzymatic activities determines the availability of active T3.
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