Biochemistry, Cellular and Molecular Biology, and Physiological Roles of the Iodothyronine Selenodeiodinases

In the citing paper

“Due to alterations in rates of local deiodination in tissues, thyroid hormone signaling can change irrespective of serum hormonal concentrations (3, 5).”

In the citing paper

“Of note, the D1 gene is upregulated by T3, and thus in hyperthyroidism the proportion of circulating T3 arising from the D1 pathway is significantly increased (11).”

In the citing paper

“A third deiodinase, type 3 deiodinase (D3) participates in the clearance of both serum T4 and T3 (11).”

In the citing paper

“The in-sufficient peripheral T3 production cannot be appropriately corrected by increasing L-T4 dose, because the inhibitory effect of elevated T4 on D2 [28,30,69] will end up increasing the imbalance of serum free T4 to free T3 ratio [67] .”

In the citing paper

“with the thyroid producing only ∼5 mcg T3”

In the citing paper

“an additional ∼25 mcg T3 is produced daily outside of the thyroid parenchyma via T4 deiodination (32).”

In the citing paper

“The daily T3 production in a 70-kg healthy adult is ∼30 mcg”

In the citing paper

“FT3 measurement has somewhat limited utility, however, in the diagnosis of hypothyroidism, since FT3 values often fall in the normal range as a result of hyperstimulation of the remaining functioning thyroid tissue by elevated TSH and to up-regulation of deiodinase D2”

In the citing paper

“Similarly, deiodinases in central and peripheral tissues are also regulated differently, enhancing T3 conversion and providing a differentiated mechanism for oversensitively responding to changes in FT4 in the feedback loop (55–63).”

In the citing paper

“T3 supply is locally controlled by several mechanisms, such as active thyroid hormone uptake, tissue-specific expression and activity of two distinct types of deiodinases converting T3 from T4, and thyroid hormone inactivation by deiodination or degradation by sulfatation, deamination, or glucoronidation (57–66).”

In the citing paper

“The regulation varies by tissue as the brain predominantly expresses type 2 deiodinase, whereas type 1 deiodinase is abundant in other tissues of the body, and by thyroid state, as T3 excess upregulates type 1 deiodinase but downregulates type 2 deiodinase, which is upregulated in hypothyroidism (57–64).”

In the citing paper

“The regulation varies by tissue as the brain predominantly expresses type 2 deiodinase, whereas type 1 deiodinase is abundant in other tissues of the body, and by thyroid state, as T3 excess upregulates type 1 deiodinase but downregulates type 2 deiodinase, which is upregulated in hypothyroidism (57–64).”

In the citing paper

“The regulation varies by tissue as the brain predominantly expresses type 2 deiodinase, whereas type 1 deiodinase is abundant in other tissues of the body, and by thyroid state, as T3 excess upregulates type 1 deiodinase but downregulates type 2 deiodinase, which is upregulated in hypothyroidism (57–64).”

In the citing paper

“the conversion of T 4 to T 3 in the brain is catalyzed by D2 (94)”

In the citing paper

“In the cortex, for example, hypothyroidism up-regulates D2 activity to produce more T 3 , whereas hyperthyroidism down-regulates D2 activity (94)”

In the citing paper

“Primarily, deiodination of T4’s outer ring by type 2 deiodinase (DIO2) gives liothyronine (L-tri-iodothyronine or T3, the main biologically active metabolite), and deiodination of the inner ring by type 1 or type 3 deiodinases (DIO1 or DIO3) gives the biologically inactive reverse T3 (rT3) [ 21 ].”