What are the two primary hormones produced and released by the thyroid gland?

The thyroid gland produces and releases two main hormones: triiodothyronine (T3) and thyroxine (T4). These hormones are essential regulators of metabolism in the body.

What is the chemical basis and essential dietary component for thyroid hormones?

Thyroid hormones, T3 and T4, are tyrosine-based hormones that are partially composed of iodine. Iodine is derived from the diet, and its deficiency leads to decreased production of these hormones.

What health condition results from a deficiency of iodine, impacting thyroid hormone production?

A deficiency in dietary iodine leads to decreased production of thyroid hormones (T3 and T4). This condition enlarges the thyroid tissue, causing a disease known as simple goiter.

Which form of thyroid hormone is most abundant in the blood, and what is its half-life?

The major form of thyroid hormone circulating in the blood is thyroxine (T4). T4 has a longer half-life, approximately one week, compared to T3.

How is the active form of thyroid hormone produced from thyroxine (T4)?

Thyroxine (T4) is converted into the more potent active form, triiodothyronine (T3), within cells by enzymes called deiodinases. T3 is estimated to be three to four times more potent than T4.

What is the significance of selenium in relation to thyroid hormone production?

Dietary selenium is essential for the production of T3, as all three isoforms of the deiodinase enzymes responsible for converting T4 to T3 contain selenium.

Is calcitonin considered a "thyroid hormone" in the typical definition?

No, calcitonin is a peptide hormone produced and secreted by the thyroid gland, but it is generally not included when referring to the 'thyroid hormones,' which specifically means T3 and T4.

How do thyroid hormones modulate energy expenditure?

Thyroid hormones modulate energy expenditure through mechanisms such as promoting mitochondrial biogenesis and stimulating adaptive thermogenesis, essentially influencing how the body uses energy.

Who was responsible for isolating thyroxine, and in what year?

American chemist Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915.

What is the medical significance of levothyroxine in the United States?

Levothyroxine, a manufactured form of thyroxine (T4), was the second most commonly prescribed medication in the United States in 2020, with over 98 million prescriptions, indicating its widespread use in medical treatment.

What are the primary functions of thyroid hormones within the body's cells?

Thyroid hormones act on nearly every cell to increase the basal metabolic rate, influence protein synthesis, support long bone growth in synergy with growth hormone, aid neural maturation, and enhance the body's sensitivity to catecholamines like adrenaline.

How do thyroid hormones affect metabolism at the cellular level?

Thyroid hormones regulate the metabolism of proteins, fats, and carbohydrates, influencing how cells utilize energy-providing compounds. They also stimulate vitamin metabolism.

What role do thyronamines play, and in what physiological processes are they involved?

Thyronamines function through an unknown mechanism to inhibit neuronal activity. They play a role in the hibernation cycles of mammals and the molting behavior of birds, and their administration can cause a significant drop in body temperature.

For what medical condition are T3 and T4 used as treatments?

Both T3 and T4 are used to treat thyroid hormone deficiency, a condition known as hypothyroidism. They are effective when taken orally due to good absorption by the stomach.

What is levothyroxine, and why is it often preferred for thyroid hormone replacement therapy?

Levothyroxine is the manufactured version of T4. It is often preferred because it is metabolized more slowly than T3, typically requiring only once-daily administration.

What are natural desiccated thyroid hormones, and what do they contain?

Natural desiccated thyroid hormones are derived from the thyroid glands of animals, primarily pigs. They are used as a natural hypothyroid treatment and contain a mixture of thyroid hormones, including T3 and T4, along with traces of T2, T1, and calcitonin.

Besides levothyroxine and natural desiccated hormones, what other formulations of thyroid hormones are available?

Other available formulations include synthetic combinations of T3 and T4 in various ratios, such as liotrix, and pure T3 medications, known as liothyronine.

What is the proposed medical use for thyronamines?

Although thyronamines currently have no established medical uses, their application has been proposed for the controlled induction of hypothermia. This could be beneficial in preventing brain damage during ischemic shock by inducing a protective cycle in the brain.

Who first synthesized thyroxine, and in what year?

Synthetic thyroxine was first successfully produced by Charles Robert Harington and George Barger in 1926.

What is the process by which thyroid hormones are synthesized within the thyroid gland?

Thyroid hormone synthesis involves several steps within the thyroid follicular cells, starting with iodide uptake, its oxidation to iodine, iodination of thyroglobulin tyrosine residues, coupling of iodinated tyrosines to form T3 and T4, endocytosis of thyroglobulin, and finally, lysosomal enzymes cleaving the hormones from thyroglobulin before they are released into the bloodstream.

What is the role of the sodium-iodide symporter in thyroid hormone synthesis?

The sodium-iodide symporter actively transports iodide ions into the thyroid follicular cells, utilizing the sodium gradient. This process, known as iodide trapping, concentrates iodide within the thyroid follicles, making it available for hormone synthesis.

What is the function of thyroglobulin in thyroid hormone production?

Thyroglobulin is a large protein precursor synthesized by thyroid follicular cells. It serves as a substrate within the thyroid follicle, where tyrosine residues on the protein are iodinated and coupled to form thyroid hormones (T3 and T4) before being released.

How does thyroid-stimulating hormone (TSH) influence thyroid hormone production?

TSH, released from the anterior pituitary, binds to receptors on the basolateral membrane of thyroid follicular cells. This binding stimulates the endocytosis of thyroglobulin from the colloid, initiating the process that leads to the release of thyroid hormones.

What is the difference between T4 and T3 in terms of activity and quantity?

Triiodothyronine (T3) is the more biologically active thyroid hormone, being three to five times more potent than thyroxine (T4). However, T4 is present in greater quantities in the blood.

What is the significance of the fetal thyroid hormone production timeline?

Fetal production of thyroxine (T4) becomes clinically significant around 18-20 weeks of gestation, and T3 levels increase later in pregnancy. This ensures the fetus has adequate thyroid hormones for proper brain development, protecting it from potential issues caused by maternal hypothyroidism.

How does the body transport thyroid hormones in the blood?

Most thyroid hormone circulating in the blood is bound to transport proteins, primarily thyroxine-binding globulin (TBG), transthyretin (TTR), and albumin. Only a small, unbound fraction (free T3 and T4) is biologically active.

Why is measuring free thyroid hormones important for diagnosis?

Measuring free T3 and free T4 is crucial for diagnosis because only the unbound hormones are biologically active. Measuring total hormone levels can be misleading due to variations in the binding proteins.

What is the approximate distribution of thyroid hormones in blood plasma?

In blood plasma, approximately 70% of thyroid hormone is bound to thyroxine-binding globulin (TBG), 10-15% to transthyretin (TTR), and 15-20% to albumin. The unbound, free forms, free T4 and free T3, constitute only about 0.03% and 0.3%, respectively.

How do thyroid hormones cross cell membranes?

Despite being lipophilic, thyroid hormones (T3 and T4) do not passively diffuse across cell membranes. Instead, they utilize carrier-mediated transport, which is an active and energy-dependent process involving specific transporters.

What is the primary mechanism by which thyroid hormones exert their effects?

Thyroid hormones primarily function by binding to nuclear receptors, known as thyroid hormone receptors. This binding influences gene transcription, affecting various cellular processes like metabolism and development.

Describe the dual mechanism of thyroid hormone action involving nuclear and cytoplasmic pathways.

Thyroid hormones act via nuclear receptors to regulate gene transcription. Additionally, a second, rapid cytoplasmic mechanism involves the TRβ receptor interacting with PI3K, influencing brain development and metabolism, a pathway conserved across mammals.

What role do thyroid hormones and iodine play in amphibian metamorphosis?

Thyroxine and iodine stimulate apoptosis (programmed cell death) in the larval gills, tail, and fins of amphibians during metamorphosis. This hormonal action facilitates the transformation from a tadpole to a frog, including changes in the nervous system.

List several key physiological effects of triiodothyronine (T3).

Triiodothyronine (T3) increases cardiac output and heart rate, boosts basal metabolic rate, enhances ventilation rate, potentiates the effects of catecholamines, supports brain development, thickens the endometrium in females, and increases the catabolism of proteins and carbohydrates.

What are the differences between measuring free and total thyroid hormones?

Measuring free T3 and free T4 provides an indication of their active levels in the body, as only the unbound hormones are biologically active. Measuring total T3 and T4 reflects both bound and unbound hormones and can be influenced by the levels of binding proteins, potentially leading to misleading results.

What is the free thyroxine index (FTI)?

The free thyroxine index (FTI) is a calculated measure used in thyroid function tests. It is derived by multiplying the total T4 level by the thyroid hormone uptake value, which estimates the amount of unbound binding sites on thyroxine-binding globulin (TBG).

What is hyperthyroidism, and what are some examples?

Hyperthyroidism is a clinical condition resulting from an excess of circulating thyroid hormones (T4 and/or T3). Graves' disease is a common example of a condition that causes hyperthyroidism.

What is hypothyroidism, and what are some examples?

Hypothyroidism occurs when there is a deficiency of thyroid hormones (T4 and/or T3). Hashimoto's thyroiditis is a common autoimmune condition that leads to hypothyroidism.

How can thyroid hormone levels be related to clinical depression?

Hypothyroidism, a state of low thyroid hormone levels, can sometimes cause clinical depression. Research suggests T3 plays a role in regulating neurotransmitters like serotonin and norepinephrine in the brain.

What cardiovascular issues can be associated with abnormal thyroid function?

Both excess (hyperthyroidism) and deficiency (hypothyroidism) of thyroid hormones can cause or exacerbate cardiovascular problems, including arrhythmias, heart failure, and atherosclerotic vascular diseases.

How can thyroid disorders affect skeletal muscles?

Abnormal thyroid function, both hypo- and hyperthyroidism, can lead to myopathies. Symptoms may include exercise-induced muscle fatigue, cramping, pain, and weakness, potentially affecting muscle fiber types and glycogen content.

What is the significance of maternal thyroid hormones during pregnancy?

Adequate maternal thyroid hormone levels are vital during pregnancy to ensure sufficient supply for the fetus and its developing brain. Untreated maternal hypothyroidism increases the risk of birth defects in the baby.

What are some examples of drugs that inhibit thyroid hormone production?

Drugs like propylthiouracil, methimazole, carbimazole, and goitrin can reduce thyroid hormone production by interfering with the oxidation of iodine, a key step in hormone synthesis.

What substances can compete with iodine for uptake into the thyroid gland?

Perchlorate and thiocyanate are substances that can compete with iodine at the sodium-iodide symporter, thereby inhibiting iodide uptake into the thyroid gland.

What is the function of the Na+/I- symporter in the thyroid gland?

The Na+/I- symporter is located on the basolateral membrane of thyroid follicular cells and actively transports iodide ions into the cells. This process is crucial for concentrating iodide, which is essential for the synthesis of thyroid hormones.

What is the role of thyroid peroxidase (TPO) in thyroid hormone synthesis?

Thyroid peroxidase (TPO) is an enzyme that oxidizes iodide ions (I-) to iodine (I0 or I2) within the thyroid follicle. It then catalyzes the iodination of tyrosine residues on thyroglobulin and the coupling of these iodinated tyrosines to form T3 and T4.

How are T1a and T0a thought to function?

T1a (iodothyronamine) and T0a (thyronamine) are positively charged and do not cross cell membranes easily. They are believed to function by interacting with the trace amine-associated receptor 1 (TAAR1), a G-protein-coupled receptor located in the cytoplasm.

What is the significance of the free thyroxine index (FTI) in thyroid testing?

The free thyroxine index (FTI) is a calculated value that helps estimate the amount of active (free) thyroxine in the blood. It is calculated by multiplying the total thyroxine (T4) level by the thyroid hormone uptake, providing a more accurate picture of thyroid hormone activity than total T4 alone.

What are the potential consequences of not taking thyroid medication as prescribed?

Failing to take prescribed thyroid medications can lead to various consequences, including the worsening of hypothyroidism symptoms and potential disruptions to normal bodily functions regulated by thyroid hormones.

What is the difference between thyrotoxicosis and hyperthyroidism?

While often used interchangeably, thyrotoxicosis refers to the clinical state of excess circulating thyroid hormones, which can be caused by intake of thyroid hormone medication or an overactive thyroid. Hyperthyroidism specifically refers to the condition caused by an overactive thyroid gland itself.

How can thyroid hormone levels affect hair growth?

Both excessive and deficient thyroid hormone levels can disrupt the normal hair growth cycle, potentially leading to hair loss. This indicates the importance of balanced thyroid function for maintaining healthy hair.

Thyroid Hormones Wiki: Thyroid Hormones: The Body's Metabolic Regulators

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What Are Thyroid Hormones?

Hormonal Duo

Thyroid hormones are two critical hormones produced and released by the thyroid gland: triiodothyronine (T₃) and thyroxine (T₄). These tyrosine-based hormones are fundamental regulators of the body's metabolic processes.^[1]

Iodine's Essential Role

Both T₃ and T₄ are synthesized using tyrosine and require iodine, which is obtained from dietary intake. A deficiency in dietary iodine impairs the production of these vital hormones, leading to an enlargement of the thyroid tissue, a condition known as simple goiter.^[2]^[3]

Bloodstream Distribution

In circulation, thyroxine (T₄) is the predominant form, with a half-life of approximately one week, significantly longer than T₃. The ratio of T₄ to T₃ released into the blood is roughly 14:1 in humans.^[4]^[5]^[6]

Metabolic Mastery

Basal Metabolic Rate

Thyroid hormones exert widespread effects across nearly every cell in the body. A primary function is to elevate the basal metabolic rate (BMR), influencing the rate at which the body consumes energy at rest.^[12]

Growth and Development

These hormones are crucial for normal development and differentiation of all body cells. They synergize with growth hormone to regulate long bone growth and are essential for proper neural maturation, particularly during fetal and early postnatal life.^[12]

Catecholamine Potentiation

Thyroid hormones increase the body's sensitivity to catecholamines, such as adrenaline (epinephrine). This "permissiveness" enhances the effects of these stress hormones, impacting cardiovascular function and the overall stress response.^[12]

Thermogenesis

Thyroid hormones stimulate heat generation within the body, contributing to thermoregulation. This is achieved through mechanisms like mitochondrial biogenesis and adaptive thermogenesis.^[7]

Hormone Synthesis Pathway

The Process Overview

Thyroid hormone synthesis is a complex, multi-step process occurring within the thyroid follicular cells, regulated by Thyroid-Stimulating Hormone (TSH) from the anterior pituitary.^[31] T₄ is converted to the more potent T₃ in peripheral tissues by deiodinase enzymes.^[53]

The synthesis involves several key stages:

Iodide Trapping: The sodium-iodide symporter (NIS) actively transports iodide ions into follicular cells, concentrating them significantly above blood levels.^[35]
Iodide Transport and Oxidation: Iodide is transported into the follicular lumen via pendrin and then oxidized by thyroid peroxidase (TPO) to reactive iodine (I⁰ or HOI).
Iodination and Coupling: Reactive iodine iodinates tyrosine residues on thyroglobulin (Tg), forming monoiodotyrosine (MIT) and diiodotyrosine (DIT). Adjacent DIT residues then couple to form T₄-yl, and MIT-DIT coupling forms T₃-yl.^[39]^[40]
Endocytosis and Hydrolysis: TSH stimulates the endocytosis of iodinated thyroglobulin. Lysosomal enzymes then cleave MIT, DIT, T₃, and T₄ from the thyroglobulin.^[43]
Hormone Release: The released thyroid hormones are transported out of the follicular cells into the bloodstream, likely involving specific transporters like MCT8 and MCT10.^[32]

Thyroglobulin itself is a large dimeric protein that serves as the scaffold for iodine attachment and hormone formation.^[46]

Fetal Development

Thyroid hormone production begins early in fetal development. The hypothalamus releases TRH by 6-8 weeks of gestation, followed by TSH from the pituitary by 12 weeks. Clinically significant T₄ levels are reached by 18-20 weeks, with T₃ levels rising later. Adequate fetal thyroid hormone levels are crucial for preventing neurodevelopmental abnormalities.^[56]

Circulation and Cellular Entry

Plasma Binding Proteins

In the bloodstream, the vast majority of thyroid hormones are bound to specific transport proteins. Only a small fraction remains unbound (free), which is the biologically active form. Measuring free hormone levels is crucial for accurate diagnosis.^[74]

Thyroid Hormone Distribution in Plasma
Type	Percentage Bound
Thyroxine-binding globulin (TBG)	~70%
Transthyretin (TTR/TBPA)	10-15%
Albumin	15-20%
Unbound T₄ (fT₄)	~0.03%
Unbound T₃ (fT₃)	~0.3%

Cellular Membrane Transport

Contrary to the lipophilic nature of hormones, thyroid hormones do not passively diffuse across cell membranes. Their transport into cells is an active, energy-dependent process mediated by at least ten identified iodothyronine transporters. This ensures that intracellular hormone concentrations can be maintained at higher levels than in the surrounding fluids.^[62]

Mechanism of Action

Nuclear Receptor Pathway

Thyroid hormones primarily exert their effects by binding to specific nuclear receptors, known as thyroid hormone receptors (TRs). These receptors, upon binding T₃ (the active form), interact with DNA sequences called thyroid hormone response elements (TREs) to regulate gene transcription, either activating or repressing gene expression.^[64]

Rapid Cytoplasmic Signaling

Emerging evidence points to a secondary, rapid mechanism involving TRs acting in the cytoplasm via the PI3K pathway. This pathway is conserved across mammals and plays a role in regulating brain development and metabolism, distinct from the classical nuclear genomic effects.^[67]^[68]

Amphibian Metamorphosis

Thyroid hormones, particularly thyroxine and iodine, are critical regulators of amphibian metamorphosis. They induce apoptosis (programmed cell death) in larval tissues like the tail and gills, facilitating the transformation from an aquatic tadpole to a terrestrial frog.^[69]

Related Endocrine Disorders

Hyperthyroidism

This condition arises from an excess of circulating free T₃ and/or T₄. It affects approximately 2% of women and 0.2% of men. Thyrotoxicosis, often used interchangeably, specifically refers to the state of excess thyroid hormones, regardless of the source (e.g., overactive gland or exogenous intake).^[79]

Hypothyroidism

Conversely, hypothyroidism results from a deficiency in T₃, T₄, or both. Examples include Hashimoto's thyroiditis. This deficiency can manifest in various ways, including neurological symptoms like clinical depression, as thyroid hormones influence neurotransmitter regulation in the brain.^[77]

Cardiovascular Impact

Both excess and deficiency of thyroid hormones can significantly impact cardiovascular health. These effects, including arrhythmias and heart failure, have been recognized for nearly two centuries.^[80]

Muscular Effects

Thyroid dysfunction can lead to myopathies, characterized by muscle fatigue, pain, and weakness. Prolonged imbalances can result in muscle fiber atrophy and altered glycogen content, impacting muscle function.^[81]^[82]

Therapeutic Approaches

Synthetic Hormones

The primary treatment for hypothyroidism is hormone replacement therapy, most commonly with synthetic thyroxine (levothyroxine). While effective, some patients report feeling better with combination therapy (levothyroxine plus synthetic T₃) or natural desiccated thyroid hormones, though clinical trials have not consistently shown superiority for these alternatives.^[13]

Monitoring and Management

Diagnosis and management of thyroid disorders rely on measuring thyroid hormone levels (total and free T₃/T₄) and TSH. Careful monitoring is essential, especially during pregnancy, where thyroid hormone needs increase.^[16]

Anti-Thyroid Drugs

For hyperthyroidism, anti-thyroid drugs like methimazole and propylthiouracil are used. These medications interfere with iodine oxidation and hormone synthesis within the thyroid gland.^[91]

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References

References used in image are found in image article in Commons:Commons:File:Thyroid system.png#References.

"Armour Thyroid", Retrieved on 1 April 2009

"Nature-Throid", Retrieved on 1 April 2009

Liothyronine

Parry CH. Elements of Pathology and Therapeutics, Being the Outlines of a Work. Bath, England: R. Cruttwell, 1815.

A full list of references for this article are available at the Thyroid hormones Wikipedia page

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Thyroid Hormones

💡 Dive in with Flashcard Learning! 💡

What Are Thyroid Hormones? 🔬

💧 Hormonal Duo

🧪 Iodine's Essential Role

⏳ Bloodstream Distribution

Metabolic Mastery ⚡

⚙️ Basal Metabolic Rate

📈 Growth and Development

💪 Catecholamine Potentiation

🔥 Thermogenesis

Hormone Synthesis Pathway 🔬

➡️ The Process Overview

👶 Fetal Development

Circulation and Cellular Entry 🚚

🔗 Plasma Binding Proteins

🚪 Cellular Membrane Transport

Mechanism of Action 🎯

💡 Nuclear Receptor Pathway

🔄 Rapid Cytoplasmic Signaling

🐸 Amphibian Metamorphosis

Related Endocrine Disorders ⚠️

⬆️ Hyperthyroidism

⬇️ Hypothyroidism

❤️ Cardiovascular Impact

💪 Muscular Effects

Therapeutic Approaches 💊

💊 Synthetic Hormones

🔬 Monitoring and Management

🚫 Anti-Thyroid Drugs

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📜 Important Notice

Dive in with Flashcard Learning!

What Are Thyroid Hormones?

Hormonal Duo

Iodine's Essential Role

Bloodstream Distribution

Metabolic Mastery

Basal Metabolic Rate

Growth and Development

Catecholamine Potentiation

Thermogenesis

Hormone Synthesis Pathway

The Process Overview

Fetal Development

Circulation and Cellular Entry

Plasma Binding Proteins

Cellular Membrane Transport

Mechanism of Action

Nuclear Receptor Pathway

Rapid Cytoplasmic Signaling

Amphibian Metamorphosis

Related Endocrine Disorders

Hyperthyroidism

Hypothyroidism

Cardiovascular Impact

Muscular Effects

Therapeutic Approaches

Synthetic Hormones

Monitoring and Management

Anti-Thyroid Drugs

Teacher's Corner

True or False?

Test Your Knowledge!

Gamer's Corner

Discover other topics to study!

References

Feedback & Support

Disclaimer

Important Notice