3,5-Diiodothyronine

Last updated
3,5-Diiodothyronine
3,5-Diiodothyronine.svg
Names
IUPAC name
2-Amino-3-[4-(4-hydroxyphenoxy)-3,5-diiodophenyl]propanoic acid
Identifiers
3D model (JSmol)
ChemSpider
MeSH 3,5-diiodothyronine
PubChem CID
UNII
  • InChI=1S/C15H13I2NO4/c16-11-5-8(7-13(18)15(20)21)6-12(17)14(11)22-10-3-1-9(19)2-4-10/h1-6,13,19H,7,18H2,(H,20,21)
    Key: ZHSOTLOTTDYIIK-UHFFFAOYSA-N
  • C1=CC(=CC=C1O)OC2=C(C=C(C=C2I)CC(C(=O)O)N)I
  • C1=CC(=CC=C1O)OC2=C(C=C(C=C2I)CC(C(=O)O)N)I
Properties
C15H13I2NO4
Molar mass 525.081 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

3,5-Diiodothyronine (3,5-T2) is an active thyroid hormone within the class of iodothyronines. It has two iodine atoms at positions 3 and 5 of its inner ring.

Contents

Biological effects

3,5-T2 is an active thyroid hormone. It stimulates the TR-beta receptor for thyroid hormones and thus increases energy expenditure. [1] [2] It has agonistic (thyromimetic) effects at myocardial tissue and pituitary, which results in 3,5-T2 suppressing TSH release. [3] [4] 3,5-T2 is an allosteric regulator of the cytochrome c oxidase, the complex IV of the electron transport chain. It increases its activity by preventing the interaction of adenosine triphosphate (ATP) as an allosteric inhibitor. [5]

Clinical significance

In nonthyroidal illness syndrome 3,5-T2 concentrations are increased. [6] [7] [8] [9] This could explain why patients with low T3 syndrome don't benefit from substitution therapy with thyroid hormones. [7]

Related Research Articles

<span class="mw-page-title-main">Iodothyronine deiodinase</span> Class of enzymes

Iodothyronine deiodinases (EC 1.21.99.4 and EC 1.21.99.3) are a subfamily of deiodinase enzymes important in the activation and deactivation of thyroid hormones. Thyroxine (T4), the precursor of 3,5,3'-triiodothyronine (T3) is transformed into T3 by deiodinase activity. T3, through binding a nuclear thyroid hormone receptor, influences the expression of genes in practically every vertebrate cell. Iodothyronine deiodinases are unusual in that these enzymes contain selenium, in the form of an otherwise rare amino acid selenocysteine.

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.

<span class="mw-page-title-main">Triiodothyronine</span> Chemical compound

Triiodothyronine, also known as T3, is a thyroid hormone. It affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate.

Thyroid function tests (TFTs) is a collective term for blood tests used to check the function of the thyroid. TFTs may be requested if a patient is thought to suffer from hyperthyroidism or hypothyroidism, or to monitor the effectiveness of either thyroid-suppression or hormone replacement therapy. It is also requested routinely in conditions linked to thyroid disease, such as atrial fibrillation and anxiety disorder.

<span class="mw-page-title-main">Thyroxine 5-deiodinase</span> Protein-coding gene in the species Homo sapiens

Thyroxine 5-deiodinase also known as type III iodothyronine deiodinase (EC number 1.21.99.3) is an enzyme that in humans is encoded by the DIO3 gene. This enzyme catalyses the following chemical reaction

The thyroid hormone receptor (TR) is a type of nuclear receptor that is activated by binding thyroid hormone. TRs act as transcription factors, ultimately affecting the regulation of gene transcription and translation. These receptors also have non-genomic effects that lead to second messenger activation, and corresponding cellular response.

<span class="mw-page-title-main">Endocrine disease</span> Medical condition

Endocrine diseases are disorders of the endocrine system. The branch of medicine associated with endocrine disorders is known as endocrinology.

<span class="mw-page-title-main">Hypothalamic–pituitary–thyroid axis</span> Part of the neuroendocrine system

The hypothalamic–pituitary–thyroid axis is part of the neuroendocrine system responsible for the regulation of metabolism and also responds to stress.

<span class="mw-page-title-main">Reverse triiodothyronine</span> Chemical compound

Reverse triiodothyronine (3,3′,5′-triiodothyronine, reverse T3, or rT3) is an isomer of triiodothyronine (3,5,3′ triiodothyronine, T3).

Euthyroid sick syndrome (ESS) is a state of adaptation or dysregulation of thyrotropic feedback control wherein the levels of T3 and/or T4 are abnormal, but the thyroid gland does not appear to be dysfunctional. This condition may result from allostatic responses of hypothalamus-pituitary-thyroid feedback control, dyshomeostatic disorders, drug interferences, and impaired assay characteristics in critical illness.

<span class="mw-page-title-main">Allan–Herndon–Dudley syndrome</span> Medical condition

Allan–Herndon–Dudley syndrome is a rare X-linked inherited disorder of brain development that causes both moderate to severe intellectual disability and problems with speech and movement.

Myxedema coma is an extreme or decompensated form of hypothyroidism and while uncommon, is potentially lethal. A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event precipitates the myxedema coma state, usually in the elderly. Primary symptoms of myxedema coma are altered mental status and low body temperature. Low blood sugar, low blood pressure, hyponatremia, hypercapnia, hypoxia, slowed heart rate, and hypoventilation may also occur. Myxedema, although included in the name, is not necessarily seen in myxedema coma. Coma is also not necessarily seen in myxedema coma, as patients may be obtunded without being comatose.

<span class="mw-page-title-main">Iodotyrosine deiodinase</span> Protein-coding gene in the species Homo sapiens

Iodotyrosine deiodinase, also known as iodotyrosine dehalogenase 1, is a type of deiodinase enzyme that scavenges iodide by removing it from iodinated tyrosine residues in the thyroid gland. These iodinated tyrosines are produced during thyroid hormone biosynthesis. The iodide that is scavenged by iodotyrosine deiodinase is necessary to again synthesize the thyroid hormones. After synthesis, the thyroid hormones circulate through the body to regulate metabolic rate, protein expression, and body temperature. Iodotyrosine deiodinase is thus necessary to keep levels of both iodide and thyroid hormones in balance.

Deiodinase (monodeiodinase) is a peroxidase enzyme that is involved in the activation or deactivation of thyroid hormones.

<span class="mw-page-title-main">Thyroid's secretory capacity</span>

Thyroid's secretory capacity is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit.

The sum activity of peripheral deiodinases is the maximum amount of triiodothyronine produced per time-unit under conditions of substrate saturation. It is assumed to reflect the activity of deiodinases outside the central nervous system and other isolated compartments. GD is therefore expected to reflect predominantly the activity of type I deiodinase.

Pulsatile secretion is a biochemical phenomenon observed in a wide variety of cell and tissue types, in which chemical products are secreted in a regular temporal pattern. The most common cellular products observed to be released in this manner are intercellular signaling molecules such as hormones or neurotransmitters. Examples of hormones that are secreted pulsatilely include insulin, thyrotropin, TRH, gonadotropin-releasing hormone (GnRH) and growth hormone (GH). In the nervous system, pulsatility is observed in oscillatory activity from central pattern generators. In the heart, pacemakers are able to work and secrete in a pulsatile manner. A pulsatile secretion pattern is critical to the function of many hormones in order to maintain the delicate homeostatic balance necessary for essential life processes, such as development and reproduction. Variations of the concentration in a certain frequency can be critical to hormone function, as evidenced by the case of GnRH agonists, which cause functional inhibition of the receptor for GnRH due to profound downregulation in response to constant (tonic) stimulation. Pulsatility may function to sensitize target tissues to the hormone of interest and upregulate receptors, leading to improved responses. This heightened response may have served to improve the animal's fitness in its environment and promote its evolutionary retention.

<span class="mw-page-title-main">Jostel's TSH index</span>

Jostel's TSH index, also referred to as Jostel's thyrotropin index or Thyroid Function index (TFI), is a method for estimating the thyrotropic function of the anterior pituitary lobe in a quantitative way. The equation has been derived from the logarithmic standard model of thyroid homeostasis. In a paper from 2014 further study was suggested to show if it is useful, but the 2018 guideline by the European Thyroid Association for the diagnosis of uncertain cases of central hypothyroidism regarded it as beneficial. It is also recommended for purposes of differential diagnosis in the sociomedical expert assessment.

<span class="mw-page-title-main">SimThyr</span> Medical research simulation software

SimThyr is a free continuous dynamic simulation program for the pituitary-thyroid feedback control system. The open-source program is based on a nonlinear model of thyroid homeostasis. In addition to simulations in the time domain the software supports various methods of sensitivity analysis. Its simulation engine is multi-threaded and supports multiple processor cores. SimThyr provides a GUI, which allows for visualising time series, modifying constant structure parameters of the feedback loop, storing parameter sets as XML files and exporting results of simulations in various formats that are suitable for statistical software. SimThyr is intended for both educational purposes and in-silico research.

The Thyrotroph Thyroid Hormone Sensitivity Index is a calculated structure parameter of thyroid homeostasis. It was originally developed to deliver a method for fast screening for resistance to thyroid hormone. Today it is also used to get an estimate for the set point of thyroid homeostasis, especially to assess dynamic thyrotropic adaptation of the anterior pituitary gland, including non-thyroidal illnesses.

References

  1. ↑ Goglia F (2014). "The effects of 3,5-diiodothyronine on energy balance". Frontiers in Physiology. 5: 528. doi: 10.3389/fphys.2014.00528 . PMC   4292545 . PMID   25628573.
  2. ↑ Lombardi A, Senese R, De Matteis R, Busiello RA, Cioffi F, Goglia F, Lanni A (2015). "3,5-Diiodo-L-thyronine activates brown adipose tissue thermogenesis in hypothyroid rats". PLOS ONE. 10 (2): e0116498. Bibcode:2015PLoSO..1016498L. doi: 10.1371/journal.pone.0116498 . PMC   4319745 . PMID   25658324.
  3. ↑ Padron AS, Neto RA, Pantaleão TU, de Souza dos Santos MC, Araujo RL, de Andrade BM, da Silva Leandro M, de Castro JP, Ferreira AC, de Carvalho DP (Jun 2014). "Administration of 3,5-diiodothyronine (3,5-T2) causes central hypothyroidism and stimulates thyroid-sensitive tissues". The Journal of Endocrinology. 221 (3): 415–27. doi:10.1530/JOE-13-0502. PMC   4045230 . PMID   24692290.
  4. ↑ Jonas W, Lietzow J, Wohlgemuth F, Hoefig CS, Wiedmer P, Schweizer U, Köhrle J, Schürmann A (Jan 2015). "3,5-Diiodo-L-thyronine (3,5-t2) exerts thyromimetic effects on hypothalamus-pituitary-thyroid axis, body composition, and energy metabolism in male diet-induced obese mice". Endocrinology. 156 (1): 389–99. doi:10.1210/en.2014-1604. PMC   4272399 . PMID   25322465.
  5. ↑ Arnold S.; Goglia F.; Kadenbach B. (1998). "3,5-Diiodothyronine binds to subunit Va of cytochrome-c oxidase and abolishes the allosteric inhibition of respiration by ATP". Eur. J. Biochem. 252 (2): 325–330. doi: 10.1046/j.1432-1327.1998.2520325.x . PMID   9523704.
  6. ↑ Pinna G, Meinhold H, Hiedra L, Thoma R, Hoell T, Gräf KJ, Stoltenburg-Didinger G, Eravci M, Prengel H, Brödel O, Finke R, Baumgartner A (May 1997). "Elevated 3,5-diiodothyronine concentrations in the sera of patients with nonthyroidal illnesses and brain tumors". The Journal of Clinical Endocrinology and Metabolism. 82 (5): 1535–42. doi: 10.1210/jcem.82.5.3939 . PMID   9141546.
  7. 1 2 Dietrich JW, Müller P, Schiedat F, Schlömicher M, Strauch J, Chatzitomaris A, Klein HH, Mügge A, Köhrle J, Rijntjes E, Lehmphul I (Jun 2015). "Nonthyroidal Illness Syndrome in Cardiac Illness Involves Elevated Concentrations of 3,5-Diiodothyronine and Correlates with Atrial Remodeling". European Thyroid Journal. 4 (2): 129–37. doi:10.1159/000381543. PMC   4521060 . PMID   26279999.
  8. ↑ Langouche, L; Lehmphul, I; Perre, SV; Köhrle, J; Van den Berghe, G (December 2016). "Circulating 3-T1AM and 3,5-T2 in Critically Ill Patients: A Cross-Sectional Observational Study". Thyroid. 26 (12): 1674–1680. doi:10.1089/thy.2016.0214. PMID   27676423.
  9. ↑ Chatzitomaris, Apostolos; Hoermann, Rudolf; Midgley, John E.; Hering, Steffen; Urban, Aline; Dietrich, Barbara; Abood, Assjana; Klein, Harald H.; Dietrich, Johannes W. (20 July 2017). "Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming". Frontiers in Endocrinology. 8: 163. doi: 10.3389/fendo.2017.00163 . PMC   5517413 . PMID   28775711.
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