Thyroid hormones - wikipedia Thyroid hormones This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. ( April 2016 ) The structural formula ( left ) and a space - filling model ( right ) of ( S ) - triiodothyronine ( T, also called liothyronine in the pharmaceutical industry ) The structural formula ( left ) and a space - filling model ( right ) of ( S ) - thyroxine ( T. ) The thyroid hormones are tyrosine - based hormones produced by the thyroid gland that are primarily responsible for regulation of metabolism. T and T are partially composed of iodine ( see molecular model ). A deficiency of iodine leads to decreased production of T and T, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine ( T ), which has a longer half - life than T. In humans, the ratio of T to T released into the blood is sometimes claimed to be quite high, but thyroid removal patient data suggests it to vary between 4 : 1 to 2 : 1, the average being 100 : 36 ( roughly 2.8 : 1 ). T is converted to the active T ( three to four times more potent than T ) within cells by deiodinases ( 5 ' - iodinase ). These are further processed by decarboxylation and deiodination to produce iodothyronamine ( T a ) and thyronamine ( T a ). All three isoforms of the deiodinases are selenium - containing enzymes, thus dietary selenium is essential for T production. Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915. Contents 1 Function 2 Medical use 2.1 Formulations 3 Production 3.1 Central 3.2 Peripheral 3.3 Initiation of production in fetuses 3.4 Effect of iodine deficiency on thyroid hormone synthesis 4 Circulation and transport 4.1 Plasma transport 4.2 Membrane transport 4.3 Intracellular transport 5 Mechanism of action 5.1 Thyroxine, iodine and apoptosis 5.2 Effects of triiodothyronine 6 Measurement 7 Related diseases 8 Anti-thyroid drugs 9 See also 10 References 11 External links Function The thyroid system of the thyroid hormones T3 and T4. The thyroid hormones act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth ( synergy with growth hormone ) and neural maturation, and increase the body 's sensitivity to catecholamines ( such as adrenaline ) by permissiveness. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also stimulate vitamin metabolism. Numerous physiological and pathological stimuli influence thyroid hormone synthesis. Thyroid hormone leads to heat generation in humans. However, the thyronamines function via some unknown mechanism to inhibit neuronal activity ; this plays an important role in the hibernation cycles of mammals and the moulting behaviour of birds. One effect of administering the thyronamines is a severe drop in body temperature. Medical use Both T and T are used to treat thyroid hormone deficiency ( hypothyroidism ). They are both absorbed well by the gut, so can be given orally. Levothyroxine is the pharmaceutical name of the manufactured version of T, which is metabolised more slowly than T and hence usually only needs once - daily administration. Natural desiccated thyroid hormones are derived from pig thyroid glands, and are a `` natural '' hypothyroid treatment containing 20 % T and traces of T, T and calcitonin. Also available are synthetic combinations of T / T in different ratios ( such as liotrix ) and pure - T medications ( INN : liothyronine ). Levothyroxine Sodium is usually the first course of treatment tried. Some patients feel they do better on desiccated thyroid hormones ; however, this is based on anecdotal evidence and clinical trials have not shown any benefit over the biosynthetic forms. Thyroid tablets are reported to have different effects, which can be attributed to the difference in torsional angles surrounding the reactive site of the molecule. Thyronamines have no medical usages yet, though their use has been proposed for controlled induction of hypothermia, which causes the brain to enter a protective cycle, useful in preventing damage during ischemic shock. Synthetic thyroxine was first successfully produced by Charles Robert Harington and George Barger in 1926. Formulations Today most patients are treated with levothyroxine, or a similar synthetic thyroid hormone. Different polymorphs of the compound have different solubilities and potencies. Additionally, natural thyroid hormone supplements from the dried thyroids of animals are still available. Levothyroxine contains T4 only and is therefore largely ineffective for patients unable to convert T4 to T3. These patients may choose to take natural thyroid hormone, as it contains a mixture of T4 and T3, or alternatively supplement with a synthetic T3 treatment. In these cases, synthetic liothyronine is preferred due to the potential differences between the natural thyroid products. Some studies show that the mixed therapy is beneficial to all patients, but the addition of lyothyronine contains additional side effects and the medication should be evaluated on an individual basis. Some natural thyroid hormone brands are FDA approved, but some are not. Thyroid hormones are generally well tolerated. Thyroid hormones are usually not dangerous for pregnant women or nursing mothers, but should be given under a doctor 's supervision. In fact, if a woman who is hypothyroid is left untreated, her baby is at a higher risk for birth defects. When pregnant, a woman with a low - functioning thyroid will also need to increase her dosage of thyroid hormone. One exception is that thyroid hormones may aggravate heart conditions, especially in older patients ; therefore, doctors may start these patients on a lower dose and work up to a larger one to avoid risk of heart attack. Production This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. ( April 2016 ) Central Synthesis of the thyroid hormones, as seen on an individual thyroid follicular cell : - Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the secretory pathway to enter the colloid in the lumen of the thyroid follicle by exocytosis. - Meanwhile, a sodium - iodide ( Na / I ) symporter pumps iodide ( I ) actively into the cell, which previously has crossed the endothelium by largely unknown mechanisms. - This iodide enters the follicular lumen from the cytoplasm by the transporter pendrin, in a purportedly passive manner. - In the colloid, iodide ( I ) is oxidized to iodine ( I ) by an enzyme called thyroid peroxidase. - Iodine ( I ) is very reactive and iodinates the thyroglobulin at tyrosyl residues in its protein chain ( in total containing approximately 120 tyrosyl residues ). - In conjugation, adjacent tyrosyl residues are paired together. - Thyroglobulin re-enters the follicular cell by endocytosis. - Proteolysis by various proteases liberates thyroxine and triiodothyronine molecules - Efflux of thyroxine and triiodothyronine from follicular cells, which appears to be largely through monocarboxylate transporter ( MCT ) 8 and 10, and entry into the blood. Thyroid hormones ( T and T ) are produced by the follicular cells of the thyroid gland and are regulated by TSH made by the thyrotropes of the anterior pituitary gland. The effects of T in vivo are mediated via T ( T is converted to T in target tissues ). T is 3 - to 5 - fold more active than T. Thyroxine ( 3, 5, 3 ', 5 ' - tetraiodothyronine ) is produced by follicular cells of the thyroid gland. It is produced as the precursor thyroglobulin ( this is not the same as thyroxine - binding globulin ( TBG ) ), which is cleaved by enzymes to produce active T. The steps in this process are as follows : The Na / I symporter transports two sodium ions across the basement membrane of the follicular cells along with an iodide ion. This is a secondary active transporter that utilises the concentration gradient of Na to move I against its concentration gradient. I is moved across the apical membrane into the colloid of the follicle. Thyroperoxidase oxidizes two I to form I. Iodide is non-reactive, and only the more reactive iodine is required for the next step. The thyroperoxidase iodinates the tyrosyl residues of the thyroglobulin within the colloid. The thyroglobulin was synthesised in the ER of the follicular cell and secreted into the colloid. Iodinated Thyroglobulin binds megalin for endocytosis back into cell. Thyroid - stimulating hormone ( TSH ) released from the adenohypophysis binds the TSH receptor ( a G protein - coupled receptor ) on the basolateral membrane of the cell and stimulates the endocytosis of the colloid. The endocytosed vesicles fuse with the lysosomes of the follicular cell. The lysosomal enzymes cleave the T from the iodinated thyroglobulin. The thyroid hormones cross the follicular cell membrane towards the blood vessels by an unknown mechanism. Text books have stated that diffusion is the main means of transport, but recent studies indicate that monocarboxylate transporter ( MCT ) 8 and 10 play major roles in the efflux of the thyroid hormones from the thyroid cells. Thyroglobulin ( Tg ) is a 660 kDa, dimeric protein produced by the follicular cells of the thyroid and used entirely within the thyroid gland. Thyroxine is produced by attaching iodine atoms to the ring structures of this protein 's tyrosine residues ; thyroxine ( T ) contains four iodine atoms, while triiodothyronine ( T ), otherwise identical to T, has one less iodine atom per molecule. The thyroglobulin protein accounts for approximately half of the protein content of the thyroid gland. Each thyroglobulin molecule contains approximately 100 - 120 tyrosine residues, a small number of which ( < 20 ) are subject to iodination catalysed by thyroperoxidase. The same enzyme then catalyses `` coupling '' of one modified tyrosine with another, via a free radical - mediated reaction, and when these iodinated bicyclic molecules are released by hydrolysis of the protein, T3 and T4 are the result. hence, each Tg protein molecule ultimately yields very small amounts of thyroid hormone ( experimentally observed to be on the order of 5 - 6 molecules of either T4 or T3 per original molecule of Tg ). More specifically, the monoatomic, anionic form of iodine, iodide, I ( displaystyle I ), is actively absorbed from the bloodstream by a process called iodide trapping. In this process, sodium is cotransported with iodide from the basolateral side of the membrane into the cell, and then concentrated in the thyroid follicles to about thirty times its concentration in the blood. Then, in the first reaction catalysed by the enzyme thyroperoxidase, tyrosine residues in the protein thyroglobulin are iodinated on their phenol rings, at one or both of the positions ortho to the phenolic hydroxyl group, yielding monoiodotyrosine ( MIT ) and diiodotyrosine ( DIT ), respectively. This introduces 1 - 2 atoms of the element iodine, covalently bound, per tyrosine residue. The further coupling together of two fully iodinated tyrosine residues, also catalysed by thyroperoxidase, yields the peptidic ( still peptide - bound ) precursor of thyroxine, and coupling one molecule of MIT and one molecule of DIT yields the comparable precursor of triiodothyronine : peptidic MIT + peptidic DIT → peptidic triiodothyronine ( eventually released as triiodothyronine, T ) 2 peptidic DITs → peptidic thyroxine ( eventually released as thyroxin, T ) ( Coupling of DIT to MIT in the opposite order yields a substance, r-T, which is biologically inactive. ) Hydrolysis ( cleavage to individual amino acids ) of the modified protein by proteases then liberates T3 and T4, as well as the non-coupled tyrosine derivatives MIT and DIT. The hormones T and T are the biologically active agents central to metabolic regulation. Peripheral Thyroxine is believed to be a prohormone and a reservoir for the most active and main thyroid hormone T. T is converted as required in the tissues by iodothyronine deiodinase. Deficiency of deiodinase can mimic hypothyroidism due to iodine deficiency. T is more active than T, though it is present in less quantity than T. Initiation of production in fetuses Thyrotropin - releasing hormone ( TRH ) is released from hypothalamus by 6 -- 8 weeks, and thyroid - stimulating hormone ( TSH ) secretion from fetal pituitary is evident by 12 weeks of gestation, and fetal production of thyroxine ( T ) reaches a clinically significant level at 18 -- 20 weeks. Fetal triiodothyronine ( T ) remains low ( less than 15 ng / dL ) until 30 weeks of gestation, and increases to 50 ng / dL at term. Fetal self - sufficiency of thyroid hormones protects the fetus against e.g. brain development abnormalities caused by maternal hypothyroidism. Effect of iodine deficiency on thyroid hormone synthesis This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. ( April 2016 ) If there is a deficiency of dietary iodine, the thyroid will not be able to make thyroid hormone. The lack of thyroid hormone will lead to decreased negative feedback on the pituitary, leading to increased production of thyroid - stimulating hormone, which causes the thyroid to enlarge ( the resulting medical condition is called endemic colloid goitre ; see goitre ). This has the effect of increasing the thyroid 's ability to trap more iodide, compensating for the iodine deficiency and allowing it to produce adequate amounts of thyroid hormone. Circulation and transport Plasma transport Most of the thyroid hormone circulating in the blood is bound to transport proteins. Only a very small fraction of the circulating hormone is free ( unbound ) and biologically active, hence measuring concentrations of free thyroid hormones is of great diagnostic value. When thyroid hormone is bound, it is not active, so the amount of free T / T is what is important. For this reason, measuring total thyroxine in the blood can be misleading. Type Percent bound to thyroxine - binding globulin ( TBG ) 70 % bound to transthyretin or `` thyroxine - binding prealbumin '' ( TTR or TBPA ) 10 - 15 % albumin 15 - 20 % unbound T ( fT ) 0.03 % unbound T ( fT ) 0.3 % Despite being lipophilic, T and T cross the cell membrane via carrier - mediated transport, which is ATP - dependent. T a and T a are positively charged and do not cross the membrane ; they are believed to function via the trace amine - associated receptor TAAR1 ( TAR1, TA1 ), a G - protein - coupled receptor located in the cell membrane. Another critical diagnostic tool is measurement of the amount of thyroid - stimulating hormone ( TSH ) that is present. Membrane transport Contrary to common belief, thyroid hormones can not traverse cell membranes in a passive manner like other lipophilic substances. The iodine in o - position makes the phenolic 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 guarantee that intracellular levels of thyroid hormones are higher than in blood plasma or interstitial fluids. Intracellular transport Little is known about intracellular kinetics of thyroid hormones. However, recently it could be demonstrated that the crystallin CRYM binds 3, 5, 3 ′ - triiodothyronine in vivo. Mechanism of action Main article : Thyroid hormone receptor The thyroid hormones function via a well - studied set of nuclear receptors, termed the thyroid hormone receptors. These receptors, together with corepressor molecules, bind DNA regions called thyroid hormone response elements ( TREs ) near genes. This receptor - corepressor - DNA complex can block gene transcription. When triiodothyronine ( T3 ) binds a receptor, it induces a conformational change in the receptor, displacing the corepressor from the complex. This leads to recruitment of coactivator proteins and RNA polymerase, activating transcription of the gene. Although this general functional model has considerable experimental support, there remain many open questions. Thyroxine, iodine and apoptosis Amphibian metamorphosis Thyroxine and iodine stimulate the spectacular apoptosis of the cells of the larval gills, tail and fins in amphibian metamorphosis, and stimulate the evolution of their nervous system transforming the aquatic, vegetarian tadpole into the terrestrial, carnivorous frog. In fact, amphibian frog Xenopus laevis serves as an ideal model system for the study of the mechanisms of apoptosis. Effects of triiodothyronine Effects of triiodothyronine ( T ) which is the metabolically active form : Increases cardiac output Increases heart rate Increases ventilation rate Increases basal metabolic rate Potentiates the effects of catecholamines ( i.e. increases sympathetic activity ) Potentiates brain development Thickens endometrium in females Increases catabolism of proteins and carbohydrates Measurement Further information : Thyroid function tests Thyroxine and triiodothyronine can be measured as free thyroxine and free triiodothyronine, which are indicators of thyroxine and triiodothyronine activities in the body. They can also be measured as total thyroxine and total triiodothyronine, which also depend on the thyroxine and triiodothyronine that is bound to thyroxine - binding globulin. A related parameter is the free thyroxine index, which is total thyroxine multiplied by thyroid hormone uptake, which, in turn, is a measure of the unbound thyroxine - binding globulins. Additionally, thyroid disorders can be detected prenatally using advanced imaging techniques and testing fetal hormone levels. Related diseases Both excess and deficiency of thyroxine can cause disorders. Hyperthyroidism ( an example is Graves Disease ) is the clinical syndrome caused by an excess of circulating free thyroxine, free triiodothyronine, or both. It is a common disorder that affects approximately 2 % of women and 0.2 % of men. Thyrotoxicosis is often used interchangeably with hyperthyroidism, but there are subtle differences. Although thyrotoxicosis also refers to an increase in circulating thyroid hormones, it can be caused by the intake of thyroxine tablets or by an over-active thyroid, whereas hyperthyroidism refers solely to an over-active thyroid. Hypothyroidism ( an example is Hashimoto 's thyroiditis ) is the case where there is a deficiency of thyroxine, triiodiothyronine, or both. Clinical depression can sometimes be caused by hypothyroidism. Some research has shown that T is found in the junctions of synapses, and regulates the amounts and activity of serotonin, norepinephrine, and γ - aminobutyric acid ( GABA ) in the brain. Hair loss can sometimes be attributed to a malfunction of t3 and t4. Normal hair growth cycle may be affected disrupting the hair growth. Preterm births can suffer neurodevelopmental disorders due to lack of maternal thyroid hormones, at a time when their own thyroid is unable to meet their postnatal needs. Also in normal pregnancies, adequate levels of maternal thyroid hormone are vital in order to ensure thyroid hormone availability for the fetus and its developing brain. Congenital hypothyroidism occurs in every 1 in 1600 -- 3400 newborns with most being born asymptomatic and developing related symptoms weeks after birth. Anti-thyroid drugs Iodine uptake against a concentration gradient is mediated by a sodium - iodine symporter and is linked to a sodium - potassium ATPase. Perchlorate and thiocyanate are drugs that can compete with iodine at this point. Compounds such as goitrin, carbimazole, methimazole, propylthiouracil can reduce thyroid hormone production by interfering with iodine oxidation. See also Goitre Graves - Basedow disease Hashimoto 's thyroiditis Hormone Polar T3 syndrome Thyroid gland Thyroid - stimulating hormone Thyronamines, metabolites of the thyroid hormones that act at the trace amine - associated receptor TAAR1 ( TAR1 ) References Jump up ^ Irizarry, Lisandro ( 23 April 2014 ). `` Thyroid Hormone Toxicity ''. Medscape. WedMD LLC. Retrieved 2 May 2014. Jump up ^ `` 1926 Edward C Kendall ''. 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Best Practice & Research Clinical Endocrinology & Metabolism. 28 ( 2 ) : 133 -- 150. doi : 10.1016 / j. beem. 2013.08. 005. Jump up ^ Spiegel C, Bestetti GE, Rossi GL, Blum JW ( September 1993 ). `` Normal circulating triiodothyronine concentrations are maintained despite severe hypothyroidism in growing pigs fed rapeseed presscake meal ''. Journal of Nutrition. 123 ( 9 ) : 1554 -- 61. PMID 8360780. External links Find TH response elements in DNA sequences. Triiodothyronine bound to proteins in the PDB Thyroxine bound to proteins in the PDB T4 at Lab Tests Online Thyroid hormone treatment in thyroid disease Thyroid Hormone Treatment Brochure by the American Thyroid Association Elaborate article about the use of thyroid drugs Written by an MD Thyroid Disease Manager Collection of elaborate medical articles on thyroid disease, including information on thyroid hormones Hormones Endocrine glands Hypothalamic - pituitary Hypothalamus GnRH TRH Dopamine CRH GHRH Somatostatin ( GHIH ) MCH Posterior pituitary Oxytocin Vasopressin Anterior pituitary FSH LH TSH Prolactin POMC CLIP ACTH MSH Endorphins Lipotropin GH Adrenal axis Adrenal cortex aldosterone cortisol cortisone DHEA DHEA - S androstenedione Adrenal medulla epinephrine norepinephrine Thyroid Thyroid hormone Calcitonin Thyroid axis Parathyroid PTH Gonadal axis Testis testosterone AMH inhibin Ovary estradiol progesterone activin and inhibin relaxin Placenta hCG HPL estrogen progesterone Pancreas glucagon insulin amylin somatostatin pancreatic polypeptide Pineal gland melatonin N, N - dimethyltryptamine 5 - methoxy - N, N - dimethyltryptamine Other Thymus Thymosins Thymosin α1 Beta thymosins Thymopoietin Thymulin Digestive system Stomach gastrin ghrelin Duodenum CCK Incretins GIP GLP - 1 secretin motilin VIP Ileum enteroglucagon peptide YY Liver / other Insulin - like growth factor IGF - 1 IGF - 2 Adipose tissue leptin adiponectin resistin Skeleton Osteocalcin Kidney renin EPO calcitriol prostaglandin Heart Natriuretic peptide ANP BNP Thyroid therapy ( H03 ) Thyroid hormones Levothyroxine Liothyronine Liotrix Tiratricol Thyroid gland preparations Antithyroid preparations Thyroid peroxidase inhibitors ( thioamide ) Thiouracils Propylthiouracil Methylthiouracil Benzylthiouracil Sulfur - containing imidazole derivatives : Carbimazole Methimazole Block conversion of T4 to T3 Propylthiouracil Ipodate Sodium - iodide symporter inhibitor Perchlorate ( Potassium perchlorate ) Pertechnetate ( Sodium pertechnetate ) Other Diiodotyrosine Dibromotyrosine WHO - EM Withdrawn from market Clinical trials : Phase III Never to phase III Thyroid hormone receptor modulators Receptor ( ligands ) THR Agonists : Dextrothyroxine DIMIT DITPA Eprotirome ( KB - 2115 ) KB - 141 KB - 2611 KB - 130015 Levothyroxine Liothyronine Liotrix MB - 07344 MB - 07811 MGL - 3196 ( VIA - 3196 ) Sobetirome ( GC - 1, GRX - 431 ) Thyroxine Tiratricol ( TRIAC ) Triiodothyronine Thyroid extract VK - 0214 VK - 2809 ZYT1 Antagonists : 1 - 850 NH3 Tetraiodothyroacetic acid ( Tetrac ) Transporter ( blockers ) NIS Inhibitors : Cyanogenic glycosides Perchlorates ( e.g., potassium perchlorate ) Pertechnetates ( e.g., sodium pertechnetate ) Thiocyanates Enzyme ( inhibitors ) TPO Inhibitors : Benzylthiouracil Carbimazole Genistein Methimazole Methylthiouracil Propylthiouracil Thiouracil Thiourea DIO Inhibitors : Dexpropranolol Iopanoic acid Ipodate sodium ( sodium iopodate ) Propranolol Propylthiouracil Others Iodine Iodine - 131 Selenium Thyroglobulin Tyrosine See also : Receptor / signaling modulators Nuclear receptor modulators Human trace amine - associated receptor ligands TAAR1 Agonists Endogenous Classical monoamine neurotransmitters Dopamine Histamine Norepinephrine Serotonin Trace amines 3 - Iodothyronamine 3 - Methoxytyramine N - Methylphenethylamine N - Methyltyramine m - Octopamine p - Octopamine Phenethylamine Phenylethanolamine Synephrine Tryptamine m - Tyramine p - Tyramine Synthetic Amphetamine DOB DOET 4 - Hydroxyamphetamine Isoprenaline MDA ( tenamfetamine ) MDMA ( midomafetamine ) 2 - Methylphenethylamine 3 - Methylphenethylamine 4 - Methylphenethylamine β - Methylphenethylamine Methamphetamine 3 - MMA Norfenfluramine Phentermine o - PIT Propylhexedrine RO5166017 N, N - Dimethylphenethylamine SEP - 363856 Neutral antagonists Inverse agonists EPPTB ( RO5212773 ) TAAR2 Agonists 3 - Iodothyronamine Phenethylamine Tyramine Neutral antagonists TAAR5 Agonists Dimethylethylamine Trimethylamine Neutral antagonists Inverse agonists 3 - Iodothyronamine References for all endogenous human TAAR1 ligands are provided at List of trace amines References for synthetic TAAR1 agonists can be found at TAAR1 or in the associated compound articles. For TAAR2 and TAAR5 agonists and inverse agonists, see TAAR for references. See also : Receptor / signaling modulators Retrieved from `` https://en.wikipedia.org/w/index.php?title=Thyroid_hormones&oldid=812651534 '' Categories : Iodinated tyrosine derivatives Hormones of the thyroid gland Thyroid hormone receptor agonists Thyroid Hormones of the hypothalamus - pituitary - thyroid axis Halogen - containing natural products Hidden categories : Wikipedia articles needing page number citations from April 2016 Articles needing additional references from April 2016 All articles needing additional references All articles with unsourced statements Articles with unsourced statements from April 2016 Wikipedia articles needing clarification from April 2016 Wikipedia articles that may have off - topic sections Talk Contents About Wikipedia অসমীয়া বাংলা Català Čeština Deutsch ދިވެހިބަސް Eesti Español فارسی Français Gaeilge Galego 한국어 Bahasa Indonesia Íslenska Italiano Кыргызча Magyar Nederlands 日本 語 Português Română Русский Slovenščina Српски / srpski Srpskohrvatski / српскохрватски Suomi Svenska Türkçe 中文 Edit links This page was last edited on 29 November 2017, at 02 : 19. 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Question: thyroid hormones (t3 and t4) are produced by
Answer: the follicular cells of the thyroid gland