Functions Of Iodine In The Human Body – Thyroid hormones are any hormones produced and secreted by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). These are tyrosine-based hormones that are primarily responsible for regulating metabolism. T

) inside cells by deiodinase (5′-deiodinase). They are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and tyranamine (T0a). All three isoforms of deiodinases are selenium-containing enzymes, so dietary selenium is essential for T

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In 2020, levothyroxine, a manufactured form of thyroxine, was the second most commonly prescribed drug in the United States, with more than 98 million prescriptions.

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Thyroid hormones affect almost every cell in the body. It acts to increase the basal metabolic rate, affects protein synthesis, helps regulate long bone growth (synergy with growth hormone) and nervous system maturation, and increases the body’s sensitivity to catecholamines (such as adrenaline) through resolution.

Thyroid hormones are necessary for the proper development and differentiation of all cells in the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use ergetic compounds. They also stimulate vitamin metabolism. Many physiological and pathological stimuli influence the synthesis of thyroid hormones.

Thyroid hormone causes heat in humans. However, thyronamines act through some unknown mechanism by inhibiting neuronal activity; it plays an important role in the hibernation cycles of mammals and the moulting behavior of birds. One of the consequences of taking thyronamine is a sharp drop in body temperature.

Are used to treat thyroid hormone deficiency (hypothyroidism). Both of them are well absorbed by the stomach, so they can be given orally. Levothyroxine is the pharmaceutical name for the manufactured version of T

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And hce usually requires administration only once a day. Natural Dried Thyroid Hormones are derived from the thyroid gland of a pig and are a “natural” preparation for the treatment of hypothyroidism containing 20% ​​T

Medicine (INN: liothyronine). Levothyroxine sodium is usually the first line of treatment. Some people feel they work better on desiccated thyroid hormones; however, this is based on anecdotal evidence, and clinical trials have not shown benefits of biosynthetic forms.

Thyroid pills have been reported to have different effects that can be attributed to the difference in torsion angles around the reactive site of the molecule.

Thyronamines do not yet have medical applications, although their use has been proposed for the controlled induction of hypothermia, which causes the brain to initiate a protective cycle useful in preventing damage during ischemic shock.

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In these cases, synthetic liothyronine is preferred because of the potential difference between natural thyroid products. Some studies suggest that combination therapy is beneficial for all patients, but the addition of liothyronine carries additional side effects and the medication should be evaluated individually.

Thyroid hormones are usually not dangerous for pregnant or nursing mothers, but they should be given under the supervision of a doctor. In fact, if a woman with hypothyroidism goes untreated, her baby is at greater risk of birth defects. During pregnancy, women with low thyroid function will also need to increase their thyroid hormone dosage.

One exception is that thyroid hormones can worsen heart disease, especially in older patients; that way, doctors can start these pills at a lower dose and work up to a higher dose to avoid the risk of a heart attack.

Thyroglobulin is synthesized in the rough doplasmic reticulum and follows the secretory pathway to ter colloid in the thyroid follicle membrane by exocytosis.

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This iodide separates the follicular membrane from the cytoplasm by the pdrin transporter in an apparently passive manner.

) is highly reactive and iodides thyroglobulin at tyrosyl residues in its protein chain (containing about 120 tyrosyl residues in total).

Thyroxine and triiodothyronine efflux from follicular cells, which appears to be mainly via monocarboxylate transporter (MCT) 8 and 10,

) are produced by follicular cells of the thyroid gland and are regulated by TSH, which is produced by thyrotrophs of the anterior pituitary gland. The effects of T

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Thyroxine (3, 5, 3′, 5′-tetraiodothyronine) is produced by follicular cells of the thyroid gland. It is produced as a precursor to thyroglobulin (this is not the same as thyroxine-binding globulin (TBG)), which is cleaved in the winter to produce active T

Thyroglobulin (Tg) is a 660 kDa dimeric protein produced by thyroid follicular cells and used by the thyroid gland.

Thyroxine is produced by the addition of iodine atoms to the ring structures of the tyrosine residues of this protein; thyroxine (T

Each thyroglobulin molecule contains approximately 100-120 tyrosine residues, a small number of which (<20) undergo thyroperoxidase-catalyzed iodination.

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The same zym catalyzes the “coupling” of one modified tyrosine with another via a free radical-mediated reaction, and when these iodinated bicyclic molecules are released upon protein hydrolysis, T

Thus, each thyroglobulin protein molecule ultimately yields a very small amount of thyroid hormone (experimentally observed on the order of 5-6 molecules of any T

In this process, sodium together with iodide is transported from the basolateral side of the membrane into the cell,

In the first reaction, catalyzed by the enzyme thyroperoxidase, tyrosine residues in the protein thyroglobulin are iodinated on their folate rings, in one or both positions of the ortho folate hydroxyl group, forming monoiodotyrosine (MIT) and diiodotyrosine (DIT), respectively. This introduces 1-2 atoms of elemental iodine covalently bound to the tyrosine residue.

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Further coupling of two fully iodinated tyrosine residues, also catalyzed by thyroperoxidase, gives the peptide (still peptide-bound) precursor of thyroxine, and coupling of one molecule of MIT and one molecule of DIT gives the comparable precursor triiodothyronine:

Thyroxine is believed to be a prohormone and reservoir for the most active and primary thyroid hormone, T

Thyrotropin-releasing hormone (TRH) is released from the hypothalamus at 6-8 weeks, and secretion of thyroid-stimulating hormone (TSH) from the pituitary gland of the fetus is detected at 12 weeks of pregnancy, and the production of thyroxine (T) in the fetus.

With a dietary iodine deficiency, the thyroid gland will not be able to produce thyroid hormones.

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Deficiency of thyroid hormones will result in decreased negative feedback on the pituitary gland, leading to increased production of thyrotropin-releasing hormone, resulting in an enlarged thyroid gland (the resulting disease is called demic colloid goiter; see goiter).

This increases the thyroid’s ability to take up more iodide, compensating for the iodine deficiency and allowing it to produce enough thyroid hormone.

Most of the thyroid hormone circulating in the blood is bound to transport proteins, and only a very small fraction is unbound and biologically active. Therefore, measurement of free thyroid hormone concentrations is important for diagnosis, while measurement of total levels may be misleading.

And positively charged do not cross the membrane; They are thought to function through the cytoplasmic G protein-coupled trace amine receptor TAAR1 (TAR1, TA1).

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Contrary to popular belief, thyroid hormones cannot cross cell membranes passively like other lipophilic substances. The iodine in the o-position makes the folic OH group more acidic, resulting in a negative charge at physiological pH. However, at least 10 different active, energy-dependent, and genetically regulated iodothyronine transporters have been identified in humans. They ensure that intracellular levels of thyroid hormones are higher than in blood plasma or interstitial fluid.

Little is known about the intracellular kinetics of thyroid hormones. However, CRYM crystallin could indeed be demonstrated to bind 3,5,3′-triiodothyronine in vivo.

Thyroid hormones function through a well-studied set of nuclear receptors called thyroid hormone receptors. These receptors, along with corepressor molecules, bind regions of DNA called thyroid hormone response elements (TREs) near ges. This receptor-corepressor-DNA complex can block ge transcription. triiodothyronine (T

), continues to bind to receptors. The deiodinase-catalyzed reaction removes an iodine atom from the 5′ position of the outer aromatic ring of thyroxine (T

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) binds the receptor, it induces conformational changes in the receptor, displacing the corepressor from the complex. This results in the recruitment of coactivator proteins and RNA polymerase, which activate ge transcription.

Stronger evidence has been obtained for a second mechanism of thyroid hormone action involving one of the same nuclear receptors, TRβ, which acts rapidly in the cytoplasm via PI3K.

The mechanism itself is parallel to the actions of the nuclear receptor in the nucleus: upon hormone abscission, TRβ binds to PI3K and inhibits its activity, but when the hormone binds the complex, it dissociates, PI3K activity increases, and the hormone-bound receptor diffuses into the nucleus.

Thyroxine and iodine stimulate apoptosis of larval gill, tail, and fin cells during metamorphosis of amphibians and stimulate the evolution of their nervous system, transforming an aquatic vegetarian tadpole into a terrestrial carnivorous frog. In fact, the amphibian frog Xopus laevis serves as an ideal model system for studying the mechanisms of apoptosis.

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) can be measured as free T3 and free T4, which are indicators of their activity in the body.

They can also be measured as total T3 and total T4, which depend on the amount bound to thyroxine-binding globulin (TBG).

A relative parameter is the free thyroxine index, which is total T4 multiplied by thyroid hormone uptake, which in turn is a measure of unbound TBH.

Premature births can also suffer from neurodevelopmental disorders due to a lack of thyroid hormones in the mother

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