Biosynthesis, transport, metabolism, and actions of thyroid hormones

2011 ◽  
pp. 307-321
Author(s):  
Theo J. Visser
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Iodine Intake ◽  
Thyroid Stimulating Hormone ◽  
Thyroid State ◽  
Peripheral Tissues ◽  
Healthy Humans ◽  
Inactive Metabolite ◽  
Tsh Secretion ◽  
The Brain

In healthy humans with a normal iodine intake, the thyroid follicular cells produce predominantly the prohormone thyroxine (3,3′,5,5′-tetraiodothyronine; T4), which is converted in peripheral tissues to the bioactive hormone 3,3′,5-triiodothyronine (T3) or to the inactive metabolite 3,3′,5′-triiodothyronine (reverse T3). The bioavailability of thyroid hormone in target tissues depends to a large extent on the supply of plasma T4 and T3, the activity of transporters mediating the cellular uptake and/or efflux of these hormones, as well as the activity of deiodinases and possibly other enzymes catalyzing their activation or inactivation. Thyroid function is regulated most importantly by the hypophyseal glycoprotein thyroid-stimulating hormone (TSH), also called thyrotropin. In turn, TSH secretion from the anterior pituitary is stimulated by the hypothalamic factor thyrotropin-releasing hormone (TRH). TSH secretion is down-regulated by negative feedback action of thyroid hormone on the hypothalamus and the pituitary. The contribution of locally produced T3 versus uptake of plasma T3 is much greater for some tissues such as the brain and the pituitary than for most other tissues. Plasma TSH is an important parameter for the diagnosis of thyroid dysfunction but is not representative for the thyroid state of all tissues. In this chapter various aspects will be discussed of: (a) the neuroendocrine regulation of thyroid function, (b) the biosynthesis of thyroid hormone (i.e. the prohormone T4), (c) the activation and inactivation of thyroid hormone in peripheral tissues, and (d) the mechanism by which T3 exerts it biological activity. A schematic overview of the hypothalamus– pituitary–thyroid–periphery axis is presented in Fig. 3.1.2.1.

scholarly journals Physiological variations in thyroid hormones: physiological and pathophysiological considerations

1996 ◽  
Vol 42 (1) ◽  
pp. 135-139 ◽  
Author(s):  
D A Fisher
Keyword(s):  
Thyroid Hormone ◽  
Metabolic Diseases ◽  
Iodine Intake ◽  
Hormone Production ◽  
Peripheral Tissues ◽  
Minimal Impact ◽  
Excessive Iodine ◽  
Thyroid Hormone Biosynthesis ◽  
Tsh Secretion ◽  
And Gender

Abstract Thyroid hormone production is regulated via pituitary thyrotropin (TSH) modulation of thyroxine (T4) prohormone secretion by the thyroid gland and regulation of active triiodothyronine (T3) production in peripheral tissues via metabolic events influencing activities of the iodothyronine monodeiodinase enzyme systems. Control at both levels is developmentally regulated and modified in serious nonthyroidal illness (trauma, infection, cancer, metabolic diseases). Racial and gender differences are of little significance except for the effects of placental estrogens and chorionic gonadotropin during pregnancy. There is a circadian rhythm of TSH secretion, with peak values at the onset of sleep and nadir concentrations during the afternoon hours. Peak and nadir concentrations differ by approximately +/- 50%. The effect on circulating T4 and T3 concentrations is not significant because of the large size of the extrathyroidal T4 pool. In healthy subjects there is no significant impact of body weight, physical training, body habitus, posture, immobilization, exercise, or ambulatory status on thyroid function, and no significant geographic environmental variation. Nutrition also has a minimal impact except for variation in iodine intake. Subthreshold concentrations of iodine intake are associated with increased TSH secretion, goiter, increased thyroid iodine uptake, decreased T4 production, an increased T3/T4 secretion ratio, and an increased ratio of circulating T3/T4 concentrations. Excessive iodine intake can block thyroid hormone biosynthesis by inhibiting the enzymes involved in the biosynthetic process, resulting in reduced T4 secretion, increased TSH concentrations, goiter, and hypothyroidism if the iodine excess is chronic.

THYROID FUNCTION TESTS: A REVIEW

2021 ◽  
pp. 73-76
Author(s):  
Vasudev Sankhla ◽  
Aman Deep
Keyword(s):  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Radioactive Iodine ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Function Tests ◽  
Function Tests ◽  
Tsh Secretion ◽  
Line Test ◽  
Radioactive Iodine Uptake

Thyroid function tests are one of the most common endocrine panels in general practice because a good understanding of when to order them, indications for treatment are important for the optimal treatment of thyroid dysfunction. Thyroid-stimulating hormone (TSH) should be the rst test to be performed on any patient with suspected thyroid dysfunction and in follow-up of individuals on treatment. It is useful as a rst-line test because even small changes in thyroid function are sufcient to cause a signicant increase in TSH secretion. Thyroxine levels may be assessed in a patient with hyperthyroidism, to determine the severity of hyperthyroxinemia. Antithyroid peroxidase measurements should be considered while evaluating patients with subclinical hypothyroidism and can facilitate the identication of autoimmune thyroiditis during the evaluation of nodular thyroid disease. The measurement of TSH receptor antibody must be considered when conrmation of Graves’ disease is needed and radioactive iodine uptake cannot be done.

scholarly journals AMIODARON SEBAGAI OBAT ANTI ARITMIA DAN PENGARUHNYA TERHADAP FUNGSI TIROID

2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Starry H. Rampengan
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Function ◽  
Hormone Replacement ◽  
Type I ◽  
Peripheral Tissues ◽  
Hormone Synthesis ◽  
Thyroid Hormone Metabolism ◽  
Serum T4 ◽  
Life Threatening

Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring.     Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian  hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya  disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.

Iodide Metabolism and Effects

2020 ◽  
pp. 25-33
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Dietary Supplement ◽  
Thyroid Function ◽  
Thyroid Stimulating Hormone ◽  
Hormone Synthesis ◽  
Serum Tsh ◽  
Tsh Stimulation ◽  
Sensitive Marker

Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.

Neutralization of TNF does not influence endotoxininduced changes in thyroid hormone metabolism in humans

1999 ◽  
Vol 276 (2) ◽  
pp. R357-R362 ◽  
Author(s):  
Tom van der Poll ◽  
Erik Endert ◽  
Susette M. Coyle ◽  
Jan M. Agosti ◽  
Stephen F. Lowry
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Stimulating Hormone ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Healthy Humans ◽  
Transient Rise ◽  
Induced Changes ◽  
Necrosis Factor ◽  
Control Study

To determine the role of tumor necrosis factor (TNF) in endotoxin-induced changes in plasma thyroid hormone and thyroid-stimulating hormone (TSH) concentrations, 24 healthy postabsorptive humans were studied on a control study day ( n= 6), after infusion of a recombinant TNF receptor IgG fusion protein (TNFR:Fc; 6 mg/m2; n = 6) after intravenous injection of endotoxin (2 ng/kg; n = 6), or after administration of endotoxin with TNFR:Fc ( n = 6). Administration of TNFR:Fc alone did not affect thyroid hormone or TSH levels when compared with the control day. Endotoxin induced a transient rise in plasma TNF activity (1.5 h: 219 ± 42 pg/ml), which was completely prevented by TNFR:Fc ( P < 0.05). After endotoxin administration, plasmal-thyroxine (T4), free T4, 3,5,3′-triiodothyronine (T3), and TSH were lower and 3,3′,5′-triiodothyronine was higher than on the control day (all P < 0.05). Coinfusion of TNFR:Fc with endotoxin did not influence these endotoxin-induced changes. Our results suggest that endogenous TNF does not play an important role in the alterations in plasma thyroid hormone and TSH concentrations induced by mild endotoxemia in healthy humans.

Screening for New Markers to Assess Thyroid Hormone Action by OMICs Analysis of Human Samples

2020 ◽  
Vol 128 (06/07) ◽  
pp. 479-487 ◽  
Author(s):  
Nele Friedrich ◽  
Maik Pietzner ◽  
Beatrice Engelmann ◽  
Georg Homuth ◽  
Dagmar Führer ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Clinical Symptoms ◽  
Pituitary Tumors ◽  
Population Based ◽  
Thyroid Stimulating Hormone ◽  
Central Hypothyroidism ◽  
Free Thyroid Hormones ◽  
Molecular Alterations ◽  
Novel Biomarkers

ABSTRACTDetermination of the levels of thyroid-stimulating hormone (TSH) and free thyroid hormones (fTHs) is crucial for assessing thyroid function. However, as a result of inter-individual genetic variability and different environmental factors individual set points exist for TSH and fTHs and display considerable variation. Furthermore, under specific pathophysiological conditions like central hypothyroidism, TSH secreting pituitary tumors, or thyroid hormone resistance the established markers TSH and fTH fail to reliably predict thyroid function and adequate supply of TH to peripheral organs. Even in case of overt hyper- and hypothyroidism circulating fTH concentrations do not correlate with clinical symptoms. Therefore, there is a clear need for novel, more specific biomarkers to diagnose and monitor thyroid function. OMICs screening approaches allow parallel profiling of hundreds to thousands of molecules and thus comprehensive monitoring of molecular alterations in tissues and body fluids that might be associated with changes in thyroid function. These techniques thus constitute promising tools for the identification of urgently needed novel biomarkers. This mini review summarizes the findings of OMICs studies in thyroid research with a particular focus on population-based and patient studies as well as interventional approaches investigating the effects of thyroid hormone administration.

scholarly journals Effects of maternal nicotine exposure on thyroid hormone metabolism and function in adult rat progeny

2015 ◽  
Vol 224 (3) ◽  
pp. 315-325 ◽  
Author(s):  
P C Lisboa ◽  
E de Oliveira ◽  
A C Manhães ◽  
A P Santos-Silva ◽  
C R Pinheiro ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Uncoupling Protein ◽  
Saline Control ◽  
Lower Sensitivity ◽  
Nicotine Exposure ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Tsh Secretion ◽  
And Function

Postnatal nicotine exposure leads to obesity and hypothyroidism in adulthood. We studied the effects of maternal nicotine exposure during lactation on thyroid hormone (TH) metabolism and function in adult offspring. Lactating rats received implants of osmotic minipumps releasing nicotine (NIC, 6 mg/kg per day s.c.) or saline (control) from postnatal days 2 to 16. Offspring were killed at 180 days. We measured types 1 and 2 deiodinase activity and mRNA, mitochondrial α-glycerol-3-phosphate dehydrogenase (mGPD) activity, TH receptor (TR), uncoupling protein 1 (UCP1), hypothalamic TRH, pituitary TSH, andin vitroTRH-stimulated TSH secretion. Expression of deiodinase mRNAs followed the same profile as that of the enzymatic activity. NIC exposure caused lower 5′-D1 and mGPD activities; lower TRβ1 content in liver as well as lower 5′-D1 activity in muscle; and higher 5′-D2 activity in brown adipose tissue (BAT), heart, and testis, which are in accordance with hypothyroidism. Although deiodinase activities were not changed in the hypothalamus, pituitary, and thyroid of NIC offspring, UCP1 expression was lower in BAT. Levels of both TRH and TSH were lower in offspring exposed to NIC, which presented higher basalin vitroTSH secretion, which was not increased in response to TRH. Thus, the hypothyroidism in NIC offspring at adulthood was caused, in part, byin vivoTRH–TSH suppression and lower sensitivity to TRH. Despite the hypothyroid status of peripheral tissues, these animals seem to develop an adaptive mechanism to preserve thyroxine to triiodothyronine conversion in central tissues.

scholarly journals The Role of Iodine for Thyroid Function in Lactating Women and Infants

2021 ◽  
Author(s):  
Maria Andersson ◽  
Christian P Braegger
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Iodine Deficiency ◽  
Current Knowledge ◽  
Iodine Intake ◽  
Infants And Toddlers ◽  
Iodine Nutrition ◽  
Lactating Women ◽  
Hormone Synthesis ◽  
The Impact

Abstract Iodine is a micronutrient needed for the production of thyroid hormones, which regulate metabolism, growth, and development. Iodine deficiency or excess may alter the thyroid hormone synthesis. The potential effects on infant development depend on the degree, timing, and duration of exposure. The iodine requirement is particularly high during infancy because of elevated thyroid hormone turnover. Breastfed infants rely on iodine provided by human milk, but the iodine concentration in breast milk is determined by the maternal iodine intake. Diets in many countries cannot provide sufficient iodine, and deficiency is prevented by iodine fortification of salt. However, the coverage of iodized salt varies between countries. Epidemiological data suggest large differences in the iodine intake in lactating women, infants, and toddlers worldwide, ranging from deficient to excessive intake. In this review, we provide an overview of the current knowledge and recent advances in the understanding of iodine nutrition and its association with thyroid function in lactating women, infants, and toddlers. We discuss risk factors for iodine malnutrition and the impact of targeted intervention strategies on these vulnerable population groups. We highlight the importance of appropriate definitions of optimal iodine nutrition and the need for more data assessing the risk of mild iodine deficiency for thyroid disorders during the first 2 years in life.

scholarly journals Combined effects of cadmium and decabrominated diphenyl ether on thyroid hormones in rats

2012 ◽  
Vol 63 (3) ◽  
pp. 255-262 ◽  
Author(s):  
Marijana Ćurčić ◽  
Saša Janković ◽  
Vesna Jaćević ◽  
Sanja Stanković ◽  
Slavica Vučinić ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Wistar Rats ◽  
Diphenyl Ether ◽  
Thyroid Stimulating Hormone ◽  
Combined Effects ◽  
Single Substance ◽  
Hormone Homeostasis ◽  
Stimulating Hormone

The aim of this study was to see how a mixture of cadmium (Cd) and decabrominated diphenyl ether (BDE209) affect thyroid function, namely thyroid-stimulating hormone (TSH), thyroxin (T4), free thyroxin (FT4), triiodothyronin (T3), and free triiodothyronin (FT3) in Wistar rats (eight per group) receiving either a single substance or their combination by gavage for 28 days. Three groups were receiving Cd alone in the doses of 2.5 mg kg-1, 7.5 mg kg-1, or 15 mg kg-1 b. w. a day, three groups were receiving BDE209 in the doses of 1000 mg kg-1, 2000 mg kg-1, or 4000 mg kg-1 b. w. a day, while nine groups were receiving different mixtures of Cd and BDE209 in these doses (3x3 design). The results have indicated that the Cd+BDE209 mixtures more potently disrupt thyroid hormone homeostasis than would be expected from these chemicals alone.

Possible Hypothyroidism Associated with Quetiapine

2000 ◽  
Vol 34 (4) ◽  
pp. 483-486 ◽  
Author(s):  
Brett M Feret ◽  
Charles F Caley
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
African American Woman ◽  
American Woman ◽  
Drug Regimen ◽  
Thyroid Stimulating Hormone ◽  
Subsequent Treatment ◽  
Drug Induced ◽  
Bipolar Type ◽  
Receive Treatment

OBJECTIVE: To report a case of hypothyroidism occurring after the addition of quetiapine to an existing drug regimen. CASE SUMMARY: A 46-year-old African-American woman diagnosed with schizoaffective disorder, bipolar type, and a four-year history of successfully treated hyperthyroidism, was suboptimally responsive to olanzapine treatment. Transition from olanzapine to quetiapine was initiated and, approximately two months after adding quetiapine to a standing pharmacotherapeutic regimen, the patient developed an elevated thyroid-stimulating hormone (TSH) concentration of 8.45 μU/L. A diagnosis of hypothyroidism was subsequently made, treatment with levothyroxine was initiated, and the patient's thyroid function became stable. DISCUSSION: Drug-induced hypothyroidism is known to occur with several medications. Quetiapine is an atypical antipsychotic with the potential to decrease thyroid hormone concentrations in some patients; this effect may be dose related. Despite this known adverse effect, the manufacturer of quetiapine reports that elevated TSH concentrations and subsequent treatment with thyroid hormone supplementation have occurred only rarely. We report the development of hypothyroidism in a patient who had previously received successful radioactive iodine treatment for hyperthyroidism in 1994, but who had no detected thyroid abnormalities until treatment with quetiapine was started four years later. CONCLUSIONS: Patients with compromised thyroid function who receive treatment with quetiapine may develop hypothyroidism. Appropriate care for these patients may include an increased awareness of possible hypothyroidism and consideration of thyroid function monitoring.

Sign in / Sign up

Export Citation Format

Share Document