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The Iodine Group | |
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VISSER
The elemental importance of sufficient iodine intake: a trace is not enough.Visser TJ Endocrinology. 2006 May;147(5):2095-7.
"The peripheral metabolism of thyroid hormone involves three deiodinases (3). Two deiodinases (D1 and D2) have ORD activity and are thus capable of producing T from T4. Conversion of T4 to T3 is the most efficient reaction catalyzed by D2, but this is far from true for D1, which is much more effective in the ORD of rT3 (4). In addition to expression of D1 in the thyroid gland, the enzyme is particularly abundant in liver and kidney (3). Hepatic and renal D1 are important sources of circulating T3.
"D2 is expressed in human brain, pituitary, thyroid, and skeletal muscle (3). In particular in the brain and also in the anterior pituitary, D2 is extremely important for local T3 production (3). Although modest levels of D2 are found in the normal human skeletal muscle, they appear sufficient to contribute a major part of peripheral T3 production in view of the large size of this tissue (5). The relative importance of skeletal muscle D2 for plasma T3 production increases in hypothyroidism because this is associated with a decrease in D1 expression in liver and kidney and an increase in D2 expression in skeletal muscle and other tissues (6). The opposite is true for hyperthyroidism. D1 expression is stimulated by its product T3 at the transcriptional level (3). Conversely, D2 activity is under negative control of its substrates T4 and rT3, which induce the ubiquitination and degradation of the enzyme (3)."
Biochemical mechanisms of thyroid hormone deiodination.Kuiper GG, Kester MH, Peeters RP, Visser TJ. Thyroid. 2005 Aug;15(8):787-98. Review.
"Deiodination is the foremost pathway of thyroid hormone metabolism not only in quantitative terms but also because thyroxine (T(4)) is activated by outer ring deiodination (ORD) to 3,3',5-triiodothyronine (T(3)), whereas both T(4) and T(3) are inactivated by inner ring deiodination (IRD) to 3,3',5-triiodothyronine and 3,3'-diiodothyronine, respectively. These reactions are catalyzed by three iodothyronine deiodinases, D1-3. Although they are homologous selenoproteins, they differ in important respects such as catalysis of ORD and/or IRD, deiodination of sulfated iodothyronines, inhibition by the thyrostatic drug propylthiouracil, and regulation during fetal and neonatal development, by thyroid state, and during illness. In this review we will briefly discuss recent developments in these different areas. These have resulted in the emerging view that the biological activity of thyroid hormone is regulated locally by tissue-specific regulation of the different deiodinases."
Pathways of thyroid hormone metabolism.Visser TJ. Acta Med Austriaca. 1996;23(1-2):10-6. Review.
"T4 is the main product secreted by the thyroid follicular cells and is regarded as a precursor of the bioactive hormone T3, most of which is produced by outer ring deiodination of T4 in peripheral tissues. Both T4 and T3 are inactivated by inner ring deiodination. Three deiodinases have been identified with outer and/or inner ring deiodinase activities, which play an important role in the tissue-specific regulation of thyroid hormone bioactivity. All three enzymes have recently been shown to contain selenocysteine residues. The second important pathway of thyroid hormone metabolism involves the conjugation of the phenolic hydroxyl group with sulfate or glucuronic acid. The glucuronides are excreted in bile, acting as intermediates in the enterohepatic cycle and fecal excretion of thyroid hormone. Sulfation accelerates the deiodination of different iodothyronines by the type I deiodinase and, thus, initiates the irreversible degradation of the hormone. If type I deiodinases activity is low, e.g. in the fetus, T3 sulfate may function as a reservoir from which active T3 is recovered by tissue sulfatase activity."
Thyroid function and deiodinase activities in rats with marginal iodine deficiency.Janssen KP, Van Der Heide D, Visser TJ, Kaptein E, Beynen AC. Biol Trace Elem Res. 1994 Mar;40(3):237-46.
"The hypothesis tested was whether marginal iodine deficiency for a period of 6 wk affects iodothyronine deiodinase activities in liver and brain of rats. Male rats were fed purified diets either deficient or sufficient in iodine; the diets were fed on a restricted basis (60% of ad libitum intake). Body weight gain of the two groups was comparable. Iodine deficiency was evidenced by increased thyroid weight (26%), reduced urinary iodine excretion (80%), and reduced plasma T4 concentrations (22%). Activities of liver type I and brain type III deiodinase were unchanged, but the activity of type II deiodinase in brain was increased (28%) in the iodine-deficient rats. Food restriction per se significantly lowered T3 (30%) and T4 (22%) concentrations in plasma and decreased type III deiodinase activity in brain (30%). These results indicate that in marginal iodine deficiency the activities of hepatic type I deiodinase and brain type III deiodinase are unchanged, whereas that of brain type II deiodinase is increased."
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