Location of hormones. The Intricate Relationship Between Hormones and the Immune System: A Comprehensive Analysis

27.07.197622.10.2021 by alexxlab

How do hormones influence immune responses. What role does estrogen play in autoimmunity. How do hormones affect cytokine production and immune cell function. What is the impact of hormones on dendritic cells and Toll-like receptors.

Содержание

The Complex Interplay of Hormones and Immune Function

Hormones, particularly estrogens, have long been recognized as significant contributors to immune system regulation and the development of autoimmune diseases. While their exact molecular mechanisms remain elusive, extensive research has shed light on the multifaceted ways in which hormones influence various components of the immune response.

Hormonal Effects on Immune Cells

Studies have demonstrated that hormones can impact:

Cytokine production by immune cells
Gene regulation in T cells
Immunoglobulin production by B lymphocytes
Function of granulocytes and NK cells

These effects highlight the broad reach of hormonal influence on immune system components.

Estrogen’s Role in Autoimmunity: Unveiling Molecular Mechanisms

Estrogen has emerged as a key player in autoimmune processes, with several molecular mechanisms coming to light:

B Cell Survival and Autoreactivity

How does estrogen contribute to B cell autoreactivity? Estrogen upregulates the expression of Bcl-2, an antiapoptotic molecule, promoting the survival of autoreactive B cells and allowing them to escape tolerance induction. This mechanism was observed in non-autoimmune mice transgenic for the heavy chain of a pathogenic anti-dsDNA antibody.

Antibody Affinity Maturation

Estrogen directly activates the transcription of activation-induced deaminase (AID), an enzyme crucial for somatic hypermutation and class-switch recombination in B cells. This process is essential for antibody affinity maturation, potentially contributing to the production of high-affinity autoantibodies.

T Cell Survival and Activation

How does estrogen affect T cell function in autoimmunity? Estrogen enables the survival and persistence of autoreactive T cells by:

Downregulating FasL
Suppressing activation-induced cell death of human SLE T cells
Increasing calcineurin mRNA expression and protein phosphatase 2B activity
Upregulating CD40L expression in T cells from lupus patients

These effects collectively contribute to enhanced T cell survival and activation in autoimmune conditions.

Hormonal Regulation of Cytokine Production: Implications for Immune Responses

Cytokines play a crucial role in shaping immune responses, and hormones significantly influence their production and balance.

Estrogen and Cytokine Profiles

How does estrogen modulate cytokine production? Estrogen has been shown to:

Promote Th2 cytokine production (IL-4, IL-10, TGFβ) at high doses
Correlate with low IL-2 levels in lupus-prone mice
Increase TNF and IL-6 levels after LPS challenge in normal and lupus-prone mice
Enhance IL-17 production in splenocytes
Regulate IFNγ production and promote Th1 responses

These effects demonstrate estrogen’s complex influence on cytokine profiles, potentially contributing to the aberrant immune responses observed in autoimmune diseases.

Dendritic Cells: A Key Target of Hormonal Modulation

Dendritic cells (DCs) serve as crucial initiators of both innate and adaptive immune responses. Hormones, particularly estrogen, can significantly impact DC function and differentiation.

Estrogen’s Effects on Dendritic Cells

How does estrogen modulate dendritic cell function? Estrogen can:

Alter the expression of MHC proteins and costimulatory molecules
Regulate TLR expression
Influence cytokine production by DCs directly or indirectly
Modulate DC migratory function through changes in cytokine or chemokine production
Promote the activation and differentiation of Langerhans cell-like DCs

These effects highlight the significant impact of estrogen on DC function and its potential role in shaping immune responses.

Toll-like Receptors: Linking Hormones and Innate Immunity

Toll-like receptors (TLRs) play a critical role in innate immunity and have been implicated in the pathogenesis of autoimmune diseases like lupus. The interplay between hormones and TLRs adds another layer of complexity to immune regulation.

TLRs in Autoimmunity

Why are TLRs important in autoimmune diseases? Studies have shown that TLR7- and TLR9-deficient lupus-prone mice exhibit reduced disease severity, indicating the significance of these receptors in lupus pathogenesis.

Hormonal Influence on TLR Expression

How do hormones affect TLR expression? While direct evidence is limited, estrogen’s ability to modulate DC function suggests a potential influence on TLR expression and signaling. This area warrants further investigation to elucidate the precise mechanisms involved.

The Estrogen-Immune System Axis: Beyond Direct Effects

While the direct effects of estrogen on immune cells and functions are well-documented, it’s important to consider the broader implications of hormonal regulation on immune responses.

Regulatory Mechanisms and Estrogen

Are there indirect ways in which estrogen influences immune function? One hypothesis suggests that the regulatory mechanisms controlling estrogen-induced excitation of the immune system may be impaired in autoimmune conditions. This concept highlights the need to explore not only the direct effects of hormones but also the intricate regulatory networks that maintain immune homeostasis.

Hormonal Fluctuations and Immune Responses

How do hormonal fluctuations impact immune function over time? The cyclic nature of hormonal changes, particularly in females, may contribute to the variability in immune responses observed in different physiological states. This temporal aspect of hormonal influence adds another layer of complexity to understanding immune regulation.

Therapeutic Implications: Harnessing Hormonal Knowledge for Immune Modulation

The intricate relationship between hormones and the immune system opens up new avenues for therapeutic interventions in autoimmune diseases and other immune-related disorders.

Selective Estrogen Receptor Modulators (SERMs)

Can modulating estrogen signaling provide therapeutic benefits? The observation that tamoxifen, a selective estrogen receptor modulator, can reverse some of the pro-inflammatory effects of estrogen in animal models suggests potential for therapeutic applications. Further research into SERMs and their immunomodulatory effects may lead to novel treatment strategies.

Personalized Hormone-Based Therapies

How can individual hormonal profiles inform treatment approaches? Understanding the specific hormonal influences on immune function in individual patients may pave the way for personalized therapeutic strategies. This approach could involve tailoring hormone-based treatments or combining hormonal modulation with existing immunotherapies.

Targeting Hormone-Responsive Immune Pathways

Can specific hormone-responsive immune pathways be targeted for therapeutic benefit? Identifying and targeting the key molecular pathways through which hormones influence immune function may provide more precise and effective treatment options for autoimmune diseases and other immune-related disorders.

The complex interplay between hormones and the immune system continues to be an area of intense research and discovery. As our understanding of these intricate relationships deepens, new opportunities for therapeutic interventions and improved management of immune-related disorders are likely to emerge. The ongoing exploration of hormonal influences on immune function promises to yield valuable insights that may revolutionize our approach to treating autoimmune diseases and other immunological conditions.

Future Directions: Unraveling the Hormonal-Immune System Puzzle

As research in this field progresses, several key areas warrant further investigation to enhance our understanding of the hormone-immune system relationship.

Sex Differences in Immune Responses

Why do many autoimmune diseases show a strong sex bias? The pronounced differences in hormonal profiles between males and females may contribute to the observed sex differences in immune responses and autoimmune disease prevalence. Further research into the specific mechanisms underlying these differences could provide crucial insights for developing sex-specific therapeutic approaches.

Hormonal Influences Across the Lifespan

How do hormonal changes throughout life impact immune function? Investigating the effects of hormonal fluctuations during puberty, pregnancy, and menopause on immune responses could shed light on the varying susceptibility to autoimmune diseases and other immune-related disorders at different life stages.

Epigenetic Regulation and Hormonal Influences

What role do epigenetic mechanisms play in mediating hormonal effects on immune function? Exploring the interplay between hormones, epigenetic modifications, and gene expression in immune cells may reveal new layers of regulation and potential therapeutic targets.

Systems Biology Approaches

How can we integrate multiple levels of hormonal and immune system data? Employing systems biology approaches to analyze the complex interactions between hormones, immune cells, and signaling pathways could provide a more comprehensive understanding of the hormone-immune system relationship.

As research in this field continues to evolve, our understanding of the intricate relationships between hormones and the immune system will undoubtedly deepen. This knowledge has the potential to revolutionize our approach to treating autoimmune diseases, enhancing vaccine efficacy, and managing a wide range of immune-related disorders. By unraveling the complex interplay between hormonal influences and immune function, we may unlock new possibilities for targeted therapies and personalized medicine in the realm of immunology.

Hormones – an overview | ScienceDirect Topics

Hormones and the Immune Response

While hormones, especially estrogens, are considered to be important contributors in the aberrations of the immune response and expression of disease, their exact molecular role and mechanisms of action are still poorly understood. Studies have shown the effect of hormones on cytokine production by various immune cells, gene regulation in T cells, immunoglobulin production by B lymphocytes and function of granulocytes and NK cells.^5,6 Some of the first direct molecular evidence into the role of estrogen in autoimmunity came from studies performed in non-autoimmune mice transgenic for the heavy chain of a pathogenic anti-dsDNA antibody. Estrogen upregulates expression of the antiapoptotic molecule Bcl-2 and promotes survival of autoreactive B cells, allowing their escape from tolerance induction.⁷ An important aspect of B-cell activation is the antibody affinity maturation, which involves somatic hypermutation and class-switch recombination, both of which require the activation-induced deaminase (AID) enzyme. ⁸ Estrogen was shown to directly activate transcription of AID through binding elements within the AID promoter.⁹ Furthermore, estrogen enables the survival and persistence of autoreactive T cells by downregulating FasL and suppressing activation-induced cell death of human SLE T cells.¹⁰

Studies performed in human peripheral blood T cells have shown that estrogen increases the expression of calcineurin mRNA and the encoded protein phosphatase (PP) 2B activity in an ER-dependent manner. PP2B induces dephosphorylation of the nuclear factor of activated T cells transcription factor and subsequent nuclear translocation and binding to target genes such as CD40L. Estrogen may contribute to the increased T cell cognate help to autoreactive B cells, as estradiol administration was shown to upregulate the expression of CD40L in T cells from lupus patients but not healthy individuals.¹¹ Exposure of normal human peripheral blood T cells to estradiol led to increased expression of the transcriptional repressor cyclic AMP response element modulator (CREM) alpha and suppression of interleukin (IL-2) cytokine production. ^12,13

Cytokine abnormalities are an important component of the aberrant immune response in patients with SLE. The immune response in SLE is characterized by a Th3 type of cytokine environment, such that cytokines IL-4, IL-6, and IL-10 are increased in serum from patients. In addition, increased serum levels of the proinflammatory cytokine IL-17 and increased proportion of Th27 differentiated cells are observed in SLE patients and thought to contribute to autoimmune disease pathogenesis.¹⁴ Estrogen is known to regulate the immune system by modulating cytokine production. High doses of estrogen are known to promote Th3 cytokine (IL-4, IL-10, TGFβ) production. High serum estrogen levels correlated with low IL-2 levels in the lupus-prone NZB/NZW mice. Furthermore, estrogen treatment increased tumor necrosis factor (TNF) and IL-6 levels after challenge with lipopolysaccharide (LPS) in both normal and lupus-prone MRL/lpr mice; these effects were reversed by the selective ER modulator tamoxifen. Animal studies have shown that mice treated with synthetic estrogen were susceptible to Listeria monocytogenes bacterial infection and their splenocytes produced less IL-2, while increased IL-17 production was seen in splenocytes from estrogen-treated mice.^15,16 Estrogen is also known to regulate the proinflammatory cytokine IFNγ and was shown to enhance CD4 responses and IFNγ producing cells from lymph nodes,¹⁷ and the Th2 differentiation transcription factor T-bet was upregulated by estrogen in murine splenocytes.¹⁸

Dendritic cells (DCs) are initiators of the innate as well as adaptive immune responses and abundantly express the pattern recognition Toll-like receptors (TLRs). TLR7- and TLR9-deficient lupus-prone mice exhibit reduced disease, indicating that TLRs are important in lupus pathogenesis. DCs are defective in SLE in both humans and mice exhibiting an overstimulated phenotype and function, with increased expression of major histocompatibility complexes (MHCs) as well as costimulatory molecules CD80/86. ¹⁹ Estrogen can modulate DC differentiation and function in several ways: alter the expression of MHC proteins, costimulatory molecules, or TLR; regulate cytokine production by DCs directly or indirectly via other cell types; and modulate migratory function through changes in cytokine or chemokine production. Furthermore, estrogen is required for the activation and differentiation of DCs, specifically those bearing features of a Langerhan cell like DC.²⁰

Besides the direct role of estrogen on the immune system, another notion is that the regulatory mechanisms that normally control the estrogen-induced excitation of the immune response may be abnormal in SLE patients. To this end, DNA microarray analysis of genes expressed in the peripheral blood mononuclear cells during the menstrual cycle of healthy women were compared to those from women with SLE and showed interesting differences. Specifically, tumor necrosis factor receptor superfamily member 14 (TNFRSF14; synonym: herpes virus entry mediator, HVEM) was increased in correlation with increasing serum estrogen levels in healthy women but not in SLE patients. TNFRSF14 is a ligand for B and T lymphocyte attenuator, an inhibitory receptor which dampens lymphocyte activation and is important in maintaining immune homeostasis. These results suggest that the mechanisms that regulate the immune activating effects of estrogen may be defective in SLE patients.²¹

Your hormones | The Pituitary Foundation

Hormones produced by the pituitary gland

The two sections of the pituitary gland produce a number of different hormones which act on different target glands or cells.

Anterior pituitary

Adrenocorticotrophic hormone (ACTH)

Thyroid-stimulating hormone (TSH)

Luteinising hormone (LH)

Follicle-stimulating hormone (FSH)

Prolactin (PRL)

Growth hormone (GH)

Melanocyte-stimulating hormone (MSH)

Posterior pituitary

Anti-diuretic hormone (ADH)

Oxytocin

Table of pituitary hormones

Hormone	Target(s)	Function
ACTH	Adrenals	Stimulates the adrenal gland to produce a hormone called cortisol. ACTH is also known as corticotrophin.
TSH	Thyroid	Stimulates the thyroid gland to secrete its own hormone, which is called thyroxine. TSH is also known as thyrotrophin.
LH & FSH	Ovaries (women) Testes (men)	Controls reproductive functioning and sexual characteristics. Stimulates the ovaries to produce oestrogen and progesterone and the testes to produce testosterone and sperm. LH and FSH are known collectively as gonadotrophins. LH is also referred to as interstitial cell stimulating hormone (ICSH) in males.
PRL	Breasts	Stimulates the breasts to produce milk. This hormone is secreted in large amounts during pregnancy and breast feeding, but is present at all times in both men and women.
GH	All cells in the body	Stimulates growth and repair. Research is currently being carried out to identify the functions of GH in adult life.
MSH		Exact role in humans is unknown.
ADH	Kidneys	Controls the blood fluid and mineral levels in the body by affecting water retention by the kidneys. This hormone is also known vasopressin or argenine vasopressin (AVP).
Oxytocin	Uterus Breasts	Affects uterine contractions in pregnancy and birth and subsequent release of breast milk.

Control of hormone production is monitored continuously and regulated using feedback loops.

You may find the Your Hormones, Society for Endocrinology webiste, useful to find out more: http://www.yourhormones.info/

Hormones produced by the Hypothalamus

The secretion of hormones from the anterior pituitary is controlled by the production of hormones by the hypothalamus. Although there are a number of different hormones they can be split into two main types:

hormones that tell the pituitary to switch on production of a hormone (a releasing hormone)

hormones that tell the pituitary to switch off production of a hormone (an inhibiting hormone).

The hormones secreted by the posterior pituitary are produced in the hypothalamus and then passed down a tube between the hypothalamus and the pituitary (the pituitary stalk) when they are then secreted into the blood.

Hormones produced by other glands in the body

In total more than 200 hormones or hormone-like substances have been discovered. In addition to the hormones listed in the table above, five of these hormones are controlled by hormones released by the pituitary.

Hormone	Organ	Function
Cortisol	Adrenals	Cortisol has a number of functions. It promotes normal metabolism, maintains blood sugar levels and blood pressure, provides resistance to stress and acts as an anti-inflammatory agent. It also plays a part in regulation of fluid balance in the body.
Thyroxine	Thyroid	Thyroxine controls many body functions, including heart rate, temperature and metabolism. It also plays a role in the metabolism of calcium in the body.
Oestrogen	Ovaries	Oestrogen facilitates growth of the tissues of the sex organs and other tissues related to reproduction. Oestrogen also acts to strengthen bones and has a protective effect on the heart.
Progesterone	Ovaries	Progesterone promotes the changes in the uterus that occur in preparation for the implantation of a fertilised ovum and prepares the breasts for milk production.
Testosterone	Testes	Testosterone is responsible for the characteristics of the masculine body, including hair growth on the face and body and muscle development. Testosterone is essential for the production of sperm and also acts to strengthen bones.

For more information about glands and hormones, as well as educational resources, visit the Society for Endocrinology’s ‘You and Your Hormones’ website

Major Endocrine Glands Names Locations Products – Endocrine System Hormones And Their Sources

The main endocrine glands are the hypothalamus, pituitary (anterior and posterior), thyroid, parathyroid, adrenal (cortex and medulla), pancreas, and gonads. All these glands together form the endocrine system.

1. The hypothalamus is an endocrine organ located in the brain. The hypothalamus synthesizes hormones such as ADH and oxytocin. The hypothalamus also synthesizes and secretes regulatory hormones that control the endocrine cells in the anterior pituitary gland such as Gonadotropin-Releasing Hormone, Thyrotropin Releasing Hormone, Growth Hormone Releasing Hormone and somatostatin.

2. The pituitary gland, sometimes called the “master gland,” is located at the base of the brain. The pituitary has two distinct regions: the anterior pituitary and the posterior pituitary.

The anterior pituitary produces seven hormones: growth hormone (GH), prolactin (PRL), thyroid-stimulating hormone (TSH), melanin-stimulating hormone (MSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH). Anterior pituitary hormones are sometimes referred to as tropic hormones because they control the functioning of other organs. While these hormones are produced by the anterior pituitary, their production is controlled by regulatory hormones produced by the hypothalamus. The antidiuretic hormone (ADH) (or vasopressin) and oxytocin are produced by neurons in the hypothalamus and transported to the posterior pituitary. They are released into the circulatory system via neural signalling from the hypothalamus. These hormones are considered to be posterior pituitary hormones even though they are produced by the hypothalamus since that is where they are released into the circulatory system.

3. The thyroid gland, one of the largest endocrine glands in the body, is located in the neck, just below the larynx and in front of the trachea. The thyroid gland produces the hormones T3 (triiodothyronine) and T4 (thyroxine). These hormones increase the metabolic activity of the body‘s cells.

4. The parathyroid glands are small endocrine glands that produce parathyroid hormone. Most people have four parathyroid glands; however, the number can vary from two to six. These glands are located on the posterior surface of the thyroid gland.

5. Adrenal glands are a pair of ductless glands located above the kidneys. The adrenal glands produce glucocorticoids and androgens, which are sex hormones that promote masculinity. Androgens are produced in small amounts by the adrenal cortex in both males and females. They do not affect sexual characteristics and may supplement sex hormones released from the gonads. The adrenal medulla contains large, irregularly-shaped cells that are closely associated with blood vessels. The adrenal glands also produce epinephrine (adrenaline) and norepinephrine (noradrenaline) in response to stress.

6. The pancreas is an elongated organ that is located between the stomach and the proximal portion of the small intestine. It contains both exocrine cells that excrete digestive enzymes and endocrine cells that release hormones. As an endocrine gland, the pancreas produces several important hormones, such as insulin and glucagon in the islets of Langerhans, which are secreted into the bloodstream to regulate blood sugar levels.

7. The pineal gland is a small endocrine gland in the brain. It is located near the center of the brain, between the two hemispheres. The main hormone produced and secreted by the pineal gland is melatonin.

8. The gonads are additional types of endocrine glands. They are the sex organs and include the male testes and female ovaries. Their main role is the production of steroid hormones. The testes produce androgens, which allow for the development of secondary sex characteristics and the production of sperm cells. The ovaries produce hormones, such as estrogen and progesterone, which cause secondary sex characteristics and prepare the body for childbirth.

Practice Questions

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MCAT Official Prep (AAMC)

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Sample Test B/B Section Passage 8 Question 43

Key Points

• The hypothalamus synthesizes hormones and transports them to the posterior pituitary gland while also synthesizing and secreting regulatory hormones that control cells in the anterior pituitary gland.

• The anterior pituitary gland, regulated by the hypothalamus, produces seven tropic hormones, growth hormone (GH), prolactin (PRL), thyroid-stimulating hormone (TSH), melanin-stimulating hormone (MSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH), which control the functioning of other organs.

• The posterior pituitary stores hormones produced by the hypothalamus (ADH and oxytocin) and release them into the bloodstream; the gland does not actually produce any hormones.

• The thyroid gland produces T3, T4 and calcitonin hormones.

• Parathyroid glands are responsible for the regulation of the body’s calcium and phosphorus levels by producing parathyroid hormone, which helps control calcium release.

• The two major hormones produced by the adrenal cortex are the mineralocorticoids, which regulate the salt and water balance, and the glucocorticoids, which can regulate blood glucose and the body’s inflammatory response.

• There are three main glucocorticoids: cortisol, corticosterone, and cortisone.

• The adrenal medulla produces the hormones epinephrine and norepinephrine; these hormones regulate heart rate, breathing rate, cardiac muscle contractions, blood pressure, and blood glucose levels.

• Glucagon and insulin are examples of hormones created by the pancreas that regulate the blood sugar levels.

• The pineal gland, a small endocrine gland in the brain, is responsible for producing hormone melatonin involved in the regulation of biological rhythms, mainly circadian rhythms.

• The gonads (the testes in males and ovaries in females) are responsible for the production of steroid hormones, such as testosterone, estrogen, and progesterone.

Key Terms

Hypothalamus: a region of the forebrain located below the thalamus that regulates body temperature, some metabolic processes and governs the autonomic nervous system

Glucocorticoid: any of a group of steroid hormones, produced by the adrenal cortex, that are involved in metabolism and have anti-inflammatory properties

Epinephrine: (adrenaline) an amino acid-derived hormone secreted by the adrenal gland in response to stress

Islets of Langerhans: regions in the pancreas that contain its endocrine cells

Exocrine: producing external secretions that are released through a duct

Androgen: the generic term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of masculine characteristics in vertebrates.

Oxytocin: a hormone that stimulates contractions during labor, and then the production of milk

Antidiuretic hormone: a hormone secreted by the hypothalamus to control water levels in the body

Parathyroid hormone: a hormone secreted by the parathyroid glands that regulate the calcium concentration of blood

Melatonin: a hormone that regulates the sleep-wake cycle

Hormones, Receptors and Target Cells

What exactly are hormones and how are they different from “non-hormones”? Hormones are chemical messengers secreted into blood or extracellular fluid by one cell that affect the functioning of other cells.

Most hormones circulate in blood, coming into contact with essentially all cells. However, a given hormone usually affects only a limited number of cells, which are called target cells. A target cell responds to a hormone because it bears receptors for the hormone.

In other words, a particular cell is a target cell for a hormone if it contains functional receptors for that hormone, and cells which do not have such a receptor cannot be influenced directly by that hormone. Reception of a radio broadcast provides a good analogy. Everyone within range of a transmitter for National Public Radio is exposed to that signal (even if they don’t contribute!). However, in order to be a NPR target and thus influenced directly by their broadcasts, you have to have a receiver tuned to that frequency.

Hormone receptors are found either exposed on the surface of the cell or within the cell, depending on the type of hormone. In very basic terms, binding of hormone to receptor triggers a cascade of reactions within the cell that affects function. Additional details about receptor structure and function are provided in the section on hormone mechanism of action.

A traditional part of the definition of hormones described them as being secreted into blood and affecting cells at distant sites. However, many of the hormones known to act in that manner have been shown to also affect neighboring cells or even have effects on the same cells that secreted the hormone. Nonetheless, it is useful to be able to describe how the signal is distributed for a particular hormonal pathway, and three actions are defined:

Endocrine action: the hormone is distributed in blood and binds to distant target cells.
Paracrine action: the hormone acts locally by diffusing from its source to target cells in the neighborhood.
Autocrine action: the hormone acts on the same cell that produced it.

Two important terms are used to refer to molecules that bind to the hormone-binding sites of receptors:

Agonists are molecules that bind the receptor and induce all the post-receptor events that lead to a biologic effect. In other words, they act like the “normal” hormone, although perhaps more or less potently. Natural hormones are themselves agonists and, in many cases, more than one distinct hormone binds to the same receptor. For a given receptor, different agonists can have dramatically different potencies.
Antagonists are molecules that bind the receptor and block binding of the agonist, but fail to trigger intracellular signalling events. Antagonists are like certain types of bureaucrats – they don’t themselves perform useful work, but block the activities of those that do have the capacity to contribute. Hormone antagonists are widely used as drugs.

Finally, a comment on the names given hormones and what some have called the tyranny of terminology. Hormones are inevitably named shortly after their discovery, when understanding is necessarily rudimentary. They are often named for the first physiologic effect observed or for their major site of synthesis. As knowledge and understanding of the hormone grow, the original name often appears inappropriate or too restrictive, but it has become entrenched in the literature and is rarely changed. In other situations, a single hormone will be referred to by more than one name. The problem is that the names given to hormones often end up being either confusing or misleading. The solution is to view names as identifiers rather than strict guidelines to source or function.

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Hormones – Anatomy and Physiology

The message a hormone sends is received by a hormone receptor, a protein located either inside the cell or within the cell membrane. The receptor will process the message by initiating other signaling events or cellular mechanisms that result in the target cell’s response. Hormone receptors recognize molecules with specific shapes and side groups, and respond only to those hormones that are recognized. The same type of receptor may be located on cells in different body tissues, and trigger somewhat different responses. Thus, the response triggered by a hormone depends not only on the hormone, but also on the target cell.

Once the target cell receives the hormone signal, it can respond in a variety of ways. The response may include the stimulation of protein synthesis, activation or deactivation of enzymes, alteration in the permeability of the cell membrane, altered rates of mitosis and cell growth, and stimulation of the secretion of products. Moreover, a single hormone may be capable of inducing different responses in a given cell.

Pathways Involving Intracellular Hormone Receptors

Intracellular hormone receptors are located inside the cell. Hormones that bind to this type of receptor must be able to cross the cell membrane. Steroid hormones are derived from cholesterol and therefore can readily diffuse through the lipid bilayer of the cell membrane to reach the intracellular receptor ((Figure)). Thyroid hormones, which contain benzene rings studded with iodine, are also lipid-soluble and can enter the cell.

The location of steroid and thyroid hormone binding differs slightly: a steroid hormone may bind to its receptor within the cytosol or within the nucleus. In either case, this binding generates a hormone-receptor complex that moves toward the chromatin in the cell nucleus and binds to a particular segment of the cell’s DNA. In contrast, thyroid hormones bind to receptors already bound to DNA. For both steroid and thyroid hormones, binding of the hormone-receptor complex with DNA triggers transcription of a target gene to mRNA, which moves to the cytosol and directs protein synthesis by ribosomes.

Binding of Lipid-Soluble Hormones

A steroid hormone directly initiates the production of proteins within a target cell. Steroid hormones easily diffuse through the cell membrane. The hormone binds to its receptor in the cytosol, forming a receptor–hormone complex. The receptor–hormone complex then enters the nucleus and binds to the target gene on the DNA. Transcription of the gene creates a messenger RNA that is translated into the desired protein within the cytoplasm.

Pathways Involving Cell Membrane Hormone Receptors

Hydrophilic, or water-soluble, hormones are unable to diffuse through the lipid bilayer of the cell membrane and must therefore pass on their message to a receptor located at the surface of the cell. Except for thyroid hormones, which are lipid-soluble, all amino acid–derived hormones bind to cell membrane receptors that are located, at least in part, on the extracellular surface of the cell membrane. Therefore, they do not directly affect the transcription of target genes, but instead initiate a signaling cascade that is carried out by a molecule called a second messenger. In this case, the hormone is called a first messenger.

The second messenger used by most hormones is cyclic adenosine monophosphate (cAMP). In the cAMP second messenger system, a water-soluble hormone binds to its receptor in the cell membrane (Step 1 in (Figure)). This receptor is associated with an intracellular component called a G protein, and binding of the hormone activates the G-protein component (Step 2). The activated G protein in turn activates an enzyme called adenylyl cyclase, also known as adenylate cyclase (Step 3), which converts adenosine triphosphate (ATP) to cAMP (Step 4). As the second messenger, cAMP activates a type of enzyme called a protein kinase that is present in the cytosol (Step 5). Activated protein kinases initiate a phosphorylation cascade, in which multiple protein kinases phosphorylate (add a phosphate group to) numerous and various cellular proteins, including other enzymes (Step 6).

Binding of Water-Soluble Hormones

Water-soluble hormones cannot diffuse through the cell membrane. These hormones must bind to a surface cell-membrane receptor. The receptor then initiates a cell-signaling pathway within the cell involving G proteins, adenylyl cyclase, the secondary messenger cyclic AMP (cAMP), and protein kinases. In the final step, these protein kinases phosphorylate proteins in the cytoplasm. This activates proteins in the cell that carry out the changes specified by the hormone.

The phosphorylation of cellular proteins can trigger a wide variety of effects, from nutrient metabolism to the synthesis of different hormones and other products. The effects vary according to the type of target cell, the G proteins and kinases involved, and the phosphorylation of proteins. Examples of hormones that use cAMP as a second messenger include calcitonin, which is important for bone construction and regulating blood calcium levels; glucagon, which plays a role in blood glucose levels; and thyroid-stimulating hormone, which causes the release of T₃ and T₄ from the thyroid gland.

Overall, the phosphorylation cascade significantly increases the efficiency, speed, and specificity of the hormonal response, as thousands of signaling events can be initiated simultaneously in response to a very low concentration of hormone in the bloodstream. However, the duration of the hormone signal is short, as cAMP is quickly deactivated by the enzyme phosphodiesterase (PDE), which is located in the cytosol. The action of PDE helps to ensure that a target cell’s response ceases quickly unless new hormones arrive at the cell membrane.

Importantly, there are also G proteins that decrease the levels of cAMP in the cell in response to hormone binding. For example, when growth hormone–inhibiting hormone (GHIH), also known as somatostatin, binds to its receptors in the pituitary gland, the level of cAMP decreases, thereby inhibiting the secretion of human growth hormone.

Not all water-soluble hormones initiate the cAMP second messenger system. One common alternative system uses calcium ions as a second messenger. In this system, G proteins activate the enzyme phospholipase C (PLC), which functions similarly to adenylyl cyclase. Once activated, PLC cleaves a membrane-bound phospholipid into two molecules: diacylglycerol (DAG) and inositol triphosphate (IP₃). Like cAMP, DAG activates protein kinases that initiate a phosphorylation cascade. At the same time, IP₃ causes calcium ions to be released from storage sites within the cytosol, such as from within the smooth endoplasmic reticulum. The calcium ions then act as second messengers in two ways: they can influence enzymatic and other cellular activities directly, or they can bind to calcium-binding proteins, the most common of which is calmodulin. Upon binding calcium, calmodulin is able to modulate protein kinase within the cell. Examples of hormones that use calcium ions as a second messenger system include angiotensin II, which helps regulate blood pressure through vasoconstriction, and growth hormone–releasing hormone (GHRH), which causes the pituitary gland to release growth hormones.

15.7D: The Posterior Pituitary – Medicine LibreTexts

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Key Points
Key Terms
Posterior Pituitary Gland
Anatomy of the Posterior Pituitary Gland
Major Hormones Secreted by the Posterior Pituitary Gland

The posterior pituitary secretes two important endocrine hormones—oxytocin and antidiuretic hormone.

Learning Objectives

Identify the location of the posterior pituitary and the hormones associated with it

Key Points

The posterior pituitary (or neurohypophysis) comprises the posterior lobe of the pituitary gland and is part of the endocrine system.
Hormones known as posterior pituitary hormones are synthesized by the hypothalamus, and include oxytocin and antidiuretic hormone.
The hormones are then stored in neurosecretory vesicles (Herring bodies) before being secreted by the posterior pituitary into the bloodstream.

Key Terms

oxytocin: A hormone that stimulates contractions during labor.
posterior pituitary: The posterior pituitary (or neurohypophysis) comprises the posterior lobe of the pituitary gland and is part of the endocrine system. Despite its name, the posterior pituitary gland is not a true gland; rather, it is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary gland.
Antidiuretic hormone: A hormone that stimulates water re-absorption in the kidneys.

Posterior Pituitary Gland

Pituitary: Pituitary gland representation.

The posterior pituitary (or neurohypophysis) comprises the posterior lobe of the pituitary gland and is part of the endocrine system. Despite its name, the posterior pituitary gland is not a gland; rather, it is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary gland.

The posterior pituitary consists mainly of neuronal projections ( axons ) extending from the supraoptic and paraventricular nuclei of the hypothalamus. These axons release peptide hormones into the capillaries of the hypophyseal circulation. These are then stored in neurosecretory vesicles (Herring bodies) before being secreted by the posterior pituitary into the systemic bloodstream.

Anatomy of the Posterior Pituitary Gland

The posterior pituitary is derived from the hypothalamus and is distinct from the more fleshy, vascularized anterior lobe. The posterior pituitary is composed of two parts:

The pars nervosa, also called the neural lobe or posterior lobe, constitutes the majority of the posterior pituitary and is the storage site of oxytocin and vasopressin.
The infundibular stalk, also known as the infundibulum or pituitary stalk, bridges the hypothalamic and hypophyseal systems.

Major Hormones Secreted by the Posterior Pituitary Gland

The posterior pituitary stores two hormones secreted by the hypothalamus for later release:

Oxytocin, most of which is released from the paraventricular nucleus in the hypothalamus. Oxytocin is one of the few hormones that create a positive feedback loop.
Antidiuretic hormone (ADH, also known as vasopressin), the majority of which is released from the supraoptic nucleus in the hypothalamus. ADH acts on the collecting ducts of the kidney to facilitate the reabsorption of water into the blood.

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17.2 Hormones – Anatomy and Physiology

Learning Objectives

By the end of this section, you will be able to:

Identify the three major classes of hormones on the basis of chemical structure
Compare and contrast intracellular and cell membrane hormone receptors
Describe signaling pathways that involve cAMP and IP3
Identify several factors that influence a target cell’s response
Discuss the role of feedback loops and humoral, hormonal, and neural stimuli in hormone control

Although a given hormone may travel throughout the body in the bloodstream, it will affect the activity only of its target cells; that is, cells with receptors for that particular hormone. Once the hormone binds to the receptor, a chain of events is initiated that leads to the target cell’s response. Hormones play a critical role in the regulation of physiological processes because of the target cell responses they regulate. These responses contribute to human reproduction, growth and development of body tissues, metabolism, fluid, and electrolyte balance, sleep, and many other body functions. The major hormones of the human body and their effects are identified in Table 17.2.

Endocrine Glands and Their Major Hormones

Endocrine gland	Associated hormones	Chemical class	Effect
Pituitary (anterior)	Growth hormone (GH)	Protein	Promotes growth of body tissues
Pituitary (anterior)	Prolactin (PRL)	Peptide	Promotes milk production
Pituitary (anterior)	Thyroid-stimulating hormone (TSH)	Glycoprotein	Stimulates thyroid hormone release
Pituitary (anterior)	Adrenocorticotropic hormone (ACTH)	Peptide	Stimulates hormone release by adrenal cortex
Pituitary (anterior)	Follicle-stimulating hormone (FSH)	Glycoprotein	Stimulates gamete production
Pituitary (anterior)	Luteinizing hormone (LH)	Glycoprotein	Stimulates androgen production by gonads
Pituitary (posterior)	Antidiuretic hormone (ADH)	Peptide	Stimulates water reabsorption by kidneys
Pituitary (posterior)	Oxytocin	Peptide	Stimulates uterine contractions during childbirth
Thyroid	Thyroxine (T₄), triiodothyronine (T₃)	Amine	Stimulate basal metabolic rate
Thyroid	Calcitonin	Peptide	Reduces blood Ca²⁺ levels
Parathyroid	Parathyroid hormone (PTH)	Peptide	Increases blood Ca²⁺levels
Adrenal (cortex)	Aldosterone	Steroid	Increases blood Na⁺ levels
Adrenal (cortex)	Cortisol, corticosterone, cortisone	Steroid	Increase blood glucose levels
Adrenal (medulla)	Epinephrine, norepinephrine	Amine	Stimulate fight-or-flight response
Pineal	Melatonin	Amine	Regulates sleep cycles
Pancreas	Insulin	Protein	Reduces blood glucose levels
Pancreas	Glucagon	Protein	Increases blood glucose levels
Testes	Testosterone	Steroid	Stimulates development of male secondary sex characteristics and sperm production
Ovaries	Estrogens and progesterone	Steroid	Stimulate development of female secondary sex characteristics and prepare the body for childbirth

Table 17.2

Types of Hormones

The hormones of the human body can be divided into two major groups on the basis of their chemical structure. Hormones derived from amino acids include amines, peptides, and proteins. Those derived from lipids include steroids (Figure 17.3). These chemical groups affect a hormone’s distribution, the type of receptors it binds to, and other aspects of its function.

Figure 17.3 Amine, Peptide, Protein, and Steroid Hormone Structure

Amine Hormones

Hormones derived from the modification of amino acids are referred to as amine hormones. Typically, the original structure of the amino acid is modified such that a –COOH, or carboxyl, group is removed, whereas the −Nh4+−Nh4+, or amine, group remains.

Amine hormones are synthesized from the amino acids tryptophan or tyrosine. An example of a hormone derived from tryptophan is melatonin, which is secreted by the pineal gland and helps regulate circadian rhythm. Tyrosine derivatives include the metabolism-regulating thyroid hormones, as well as the catecholamines, such as epinephrine, norepinephrine, and dopamine. Epinephrine and norepinephrine are secreted by the adrenal medulla and play a role in the fight-or-flight response, whereas dopamine is secreted by the hypothalamus and inhibits the release of certain anterior pituitary hormones.

Peptide and Protein Hormones

Whereas the amine hormones are derived from a single amino acid, peptide and protein hormones consist of multiple amino acids that link to form an amino acid chain. Peptide hormones consist of short chains of amino acids, whereas protein hormones are longer polypeptides. Both types are synthesized like other body proteins: DNA is transcribed into mRNA, which is translated into an amino acid chain.

Examples of peptide hormones include antidiuretic hormone (ADH), a pituitary hormone important in fluid balance, and atrial-natriuretic peptide, which is produced by the heart and helps to decrease blood pressure. Some examples of protein hormones include growth hormone, which is produced by the pituitary gland, and follicle-stimulating hormone (FSH), which has an attached carbohydrate group and is thus classified as a glycoprotein. FSH helps stimulate the maturation of eggs in the ovaries and sperm in the testes.

Steroid Hormones

The primary hormones derived from lipids are steroids. Steroid hormones are derived from the lipid cholesterol. For example, the reproductive hormones testosterone and the estrogens—which are produced by the gonads (testes and ovaries)—are steroid hormones. The adrenal glands produce the steroid hormone aldosterone, which is involved in osmoregulation, and cortisol, which plays a role in metabolism.

Like cholesterol, steroid hormones are not soluble in water (they are hydrophobic). Because blood is water-based, lipid-derived hormones must travel to their target cell bound to a transport protein. This more complex structure extends the half-life of steroid hormones much longer than that of hormones derived from amino acids. A hormone’s half-life is the time required for half the concentration of the hormone to be degraded. For example, the lipid-derived hormone cortisol has a half-life of approximately 60 to 90 minutes. In contrast, the amino acid–derived hormone epinephrine has a half-life of approximately one minute.

Pathways of Hormone Action

Pathways Involving Intracellular Hormone Receptors

Intracellular hormone receptors are located inside the cell. Hormones that bind to this type of receptor must be able to cross the cell membrane. Steroid hormones are derived from cholesterol and therefore can readily diffuse through the lipid bilayer of the cell membrane to reach the intracellular receptor (Figure 17.4). Thyroid hormones, cross the cell membrane by a specific carrier-mediated mechanism that is energy and Na⁺ dependent.

Figure 17.4 Binding of Lipid-Soluble Hormones A steroid hormone directly initiates the production of proteins within a target cell. Steroid hormones easily diffuse through the cell membrane. The hormone binds to its receptor in the cytosol, forming a receptor–hormone complex. The receptor–hormone complex then enters the nucleus and binds to the target gene on the DNA. Transcription of the gene creates a messenger RNA that is translated into the desired protein within the cytoplasm.

Pathways Involving Cell Membrane Hormone Receptors

The second messenger used by most hormones is cyclic adenosine monophosphate (cAMP). In the cAMP second messenger system, a water-soluble hormone binds to its receptor in the cell membrane (Step 1 in Figure 17.5). This receptor is associated with an intracellular component called a G protein, and binding of the hormone activates the G-protein component (Step 2). The activated G protein in turn activates an enzyme called adenylyl cyclase, also known as adenylate cyclase (Step 3), which converts adenosine triphosphate (ATP) to cAMP (Step 4). As the second messenger, cAMP activates a type of enzyme called a protein kinase that is present in the cytosol (Step 5). Activated protein kinases initiate a phosphorylation cascade, in which multiple protein kinases phosphorylate (add a phosphate group to) numerous and various cellular proteins, including other enzymes (Step 6).

Figure 17.5 Binding of Water-Soluble Hormones Water-soluble hormones cannot diffuse through the cell membrane. These hormones must bind to a surface cell-membrane receptor. The receptor then initiates a cell-signaling pathway within the cell involving G proteins, adenylyl cyclase, the secondary messenger cyclic AMP (cAMP), and protein kinases. In the final step, these protein kinases phosphorylate proteins in the cytoplasm. This activates proteins in the cell that carry out the changes specified by the hormone.

Factors Affecting Target Cell Response

You will recall that target cells must have receptors specific to a given hormone if that hormone is to trigger a response. But several other factors influence the target cell response. For example, the presence of a significant level of a hormone circulating in the bloodstream can cause its target cells to decrease their number of receptors for that hormone. This process is called downregulation, and it allows cells to become less reactive to the excessive hormone levels. When the level of a hormone is chronically reduced, target cells engage in upregulation to increase their number of receptors. This process allows cells to be more sensitive to the hormone that is present. Cells can also alter the sensitivity of the receptors themselves to various hormones.

Two or more hormones can interact to affect the response of cells in a variety of ways. The three most common types of interaction are as follows:

The permissive effect, in which the presence of one hormone enables another hormone to act. For example, thyroid hormones have complex permissive relationships with certain reproductive hormones. A dietary deficiency of iodine, a component of thyroid hormones, can therefore affect reproductive system development and functioning.
The synergistic effect, in which two hormones with similar effects produce an amplified response. In some cases, two hormones are required for an adequate response. For example, two different reproductive hormones—FSH from the pituitary gland and estrogens from the ovaries—are required for the maturation of female ova (egg cells).
The antagonistic effect, in which two hormones have opposing effects. A familiar example is the effect of two pancreatic hormones, insulin and glucagon. Insulin increases the liver’s storage of glucose as glycogen, decreasing blood glucose, whereas glucagon stimulates the breakdown of glycogen stores, increasing blood glucose.

Regulation of Hormone Secretion

To prevent abnormal hormone levels and a potential disease state, hormone levels must be tightly controlled. The body maintains this control by balancing hormone production and degradation. Feedback loops govern the initiation and maintenance of most hormone secretion in response to various stimuli.

Role of Feedback Loops

The contribution of feedback loops to homeostasis will only be briefly reviewed here. Positive feedback loops are characterized by the release of additional hormone in response to an original hormone release. The release of oxytocin during childbirth is a positive feedback loop. The initial release of oxytocin begins to signal the uterine muscles to contract, which pushes the fetus toward the cervix, causing it to stretch. This, in turn, signals the pituitary gland to release more oxytocin, causing labor contractions to intensify. The release of oxytocin decreases after the birth of the child.

The more common method of hormone regulation is the negative feedback loop. Negative feedback is characterized by the inhibition of further secretion of a hormone in response to adequate levels of that hormone. This allows blood levels of the hormone to be regulated within a narrow range. An example of a negative feedback loop is the release of glucocorticoid hormones from the adrenal glands, as directed by the hypothalamus and pituitary gland. As glucocorticoid concentrations in the blood rise, the hypothalamus and pituitary gland reduce their signaling to the adrenal glands to prevent additional glucocorticoid secretion (Figure 17.6).

Figure 17.6 Negative Feedback Loop The release of adrenal glucocorticoids is stimulated by the release of hormones from the hypothalamus and pituitary gland. This signaling is inhibited when glucocorticoid levels become elevated by causing negative signals to the pituitary gland and hypothalamus.

Role of Endocrine Gland Stimuli

Reflexes triggered by both chemical and neural stimuli control endocrine activity. These reflexes may be simple, involving only one hormone response, or they may be more complex and involve many hormones, as is the case with the hypothalamic control of various anterior pituitary–controlled hormones.

Humoral stimuli are changes in blood levels of non-hormone chemicals, such as nutrients or ions, which cause the release or inhibition of a hormone to, in turn, maintain homeostasis. For example, osmoreceptors in the hypothalamus detect changes in blood osmolarity (the concentration of solutes in the blood plasma). If blood osmolarity is too high, meaning that the blood is not dilute enough, osmoreceptors signal the hypothalamus to release ADH. The hormone causes the kidneys to reabsorb more water and reduce the volume of urine produced. This reabsorption causes a reduction of the osmolarity of the blood, diluting the blood to the appropriate level. The regulation of blood glucose is another example. High blood glucose levels cause the release of insulin from the pancreas, which increases glucose uptake by cells and liver storage of glucose as glycogen.

An endocrine gland may also secrete a hormone in response to the presence of another hormone produced by a different endocrine gland. Such hormonal stimuli often involve the hypothalamus, which produces releasing and inhibiting hormones that control the secretion of a variety of pituitary hormones.

In addition to these chemical signals, hormones can also be released in response to neural stimuli. A common example of neural stimuli is the activation of the fight-or-flight response by the sympathetic nervous system. When an individual perceives danger, sympathetic neurons signal the adrenal glands to secrete norepinephrine and epinephrine. The two hormones dilate blood vessels, increase the heart and respiratory rate, and suppress the digestive and immune systems. These responses boost the body’s transport of oxygen to the brain and muscles, thereby improving the body’s ability to fight or flee.

Everyday Connection

Bisphenol A and Endocrine Disruption

You may have heard news reports about the effects of a chemical called bisphenol A (BPA) in various types of food packaging. BPA is used in the manufacturing of hard plastics and epoxy resins. Common food-related items that may contain BPA include the lining of aluminum cans, plastic food-storage containers, drinking cups, as well as baby bottles and “sippy” cups. Other uses of BPA include medical equipment, dental fillings, and the lining of water pipes.

Research suggests that BPA is an endocrine disruptor, meaning that it negatively interferes with the endocrine system, particularly during the prenatal and postnatal development period. In particular, BPA mimics the hormonal effects of estrogens and has the opposite effect—that of androgens. The U.S. Food and Drug Administration (FDA) notes in their statement about BPA safety that although traditional toxicology studies have supported the safety of low levels of exposure to BPA, recent studies using novel approaches to test for subtle effects have led to some concern about the potential effects of BPA on the brain, behavior, and prostate gland in fetuses, infants, and young children. The FDA is currently facilitating decreased use of BPA in food-related materials. Many US companies have voluntarily removed BPA from baby bottles, “sippy” cups, and the linings of infant formula cans, and most plastic reusable water bottles sold today boast that they are “BPA free.” In contrast, both Canada and the European Union have completely banned the use of BPA in baby products.

The potential harmful effects of BPA have been studied in both animal models and humans and include a large variety of health effects, such as developmental delay and disease. For example, prenatal exposure to BPA during the first trimester of human pregnancy may be associated with wheezing and aggressive behavior during childhood. Adults exposed to high levels of BPA may experience altered thyroid signaling and male sexual dysfunction. BPA exposure during the prenatal or postnatal period of development in animal models has been observed to cause neurological delays, changes in brain structure and function, sexual dysfunction, asthma, and increased risk for multiple cancers. In vitro studies have also shown that BPA exposure causes molecular changes that initiate the development of cancers of the breast, prostate, and brain. Although these studies have implicated BPA in numerous ill health effects, some experts caution that some of these studies may be flawed and that more research needs to be done. In the meantime, the FDA recommends that consumers take precautions to limit their exposure to BPA. In addition to purchasing foods in packaging free of BPA, consumers should avoid carrying or storing foods or liquids in bottles with the recycling code 3 or 7. Foods and liquids should not be microwave-heated in any form of plastic: use paper, glass, or ceramics instead.

A healthy thyroid gland is the key to harmony and beauty: POSITIVEMED

The thyroid gland is the most important endocrine organ that stores iodine and synthesizes iodine-containing hormones: thyronine (triiodothyronine or T3) , thyroxine (tetraiodothyronine) . Not only the reproductive function, the work of the digestive organs, the immune and nervous systems, but also the metabolism in the entire human body depend on the state of the thyroid gland.

Location of the thyroid gland

The gland is located in the anterior region of the neck, above the thyroid cartilage, for which it got its name.The organ consists of two lobes connected by an isthmus. The shape of the thyroid gland resembles a butterfly.

Thyroid stimulating hormone (TSH)

The thyroid gland works and develops under the influence of TSH-thyroid-stimulating hormone. This hormone is produced in the main gland of the body – the pituitary gland. The pituitary gland secretes tropic hormones that control the work of all other glands. Thus, the higher the TSH value, the more the thyroid gland is stimulated .

Thyroid function

The functions of the thyroid gland include:

iodine accumulation;
release of hormones (T3, T4 and calcitonin).

The hormone thyroxine (T4) and the hormone triiodothyronine (T3)

It is by far the main thyroid hormone. T4 is formed from the amino acid tyrosine and contains 4 iodine atoms. The hormone is activated by the cleavage of one iodine atom and conversion into T3 hormone – triiodothyronine.

Effects of thyroid hormones

Hormones affect almost all cells of the body.

Heart:

chronotropic effect – an increase in the number and affinity of beta-adrenergic receptors, and the effect on beta receptors increases the number of heart contractions and oxygen consumption by cells;
inotropic effect – an increase in the action of catecholamines – that is, adrenaline, as well as an increase in pressure and heart rate.

Adipose tissue: stimulation of lipolysis, that is, the breakdown of fats.

Muscle: protein breakdown.

Bones: growth and development of bones.

Nervous system: normalization of brain development. This function is especially important during pregnancy, since with uncompensated hypothyroidism in the mother, the fetal nervous system does not develop correctly, which can lead to various pathologies of the child’s development.

Intestine: increase in carbohydrate absorption.

The main function of hormones is to accelerate catabolism, which subsequently affects the efficiency and metabolic rate.

Hormone calcitonin

The thyroid gland also has C-cells that secrete a hormone of a peptide nature – calcitonin . This hormone is responsible for calcium-phosphorus metabolism and bone formation in our body. Calcitonin is important as a tumor marker for medullary cancer of the thyroid gland is a very dangerous, rapidly growing and metastatic cancer.In this cancer, calcitonin rises. With a decrease in calcitonin, nothing terrible happens, so people after removal of the thyroid gland for certain reasons live quietly, the level of calcium in the blood is maintained by parathyroid hormone – the hormone of the parathyroid gland.

Symptoms of thyroid gland damage

Thyrotoxicosis – when the thyroid gland secretes too much hormones. Accordingly, the metabolism accelerates. The main symptoms of thyrotoxicosis:

increased sweating, hot flashes
Decreased muscle mass
shortness of breath
Breast augmentation and gynecoastia in men
unmotivated weight loss
tachycardia
Menstrual irregularities
pretibial mexidema (edema)
nervousness, irritability
arrhythmia
increased appetite
tremor
muscle weakness
Poor condition of nails

Hypothyroidism – a decrease in the function of the thyroid gland, when it produces less hormones than is necessary, or does not produce them at all.Symptoms of hypothyroidism depend on the severity and are very nonspecific. With mild hypothyroidism, a person may not complain about anything at all. With more pronounced, it is noted:

Hair loss, especially in the eyebrow area
fluid retention, edema
feeling of chilliness and cold
reduced sweating
dry skin

In severe hypothyroidism:

the appearance of yellowness of the skin
weakness, lethargy, drowsiness
Memory Impairment
cognitive decline
rare heart rate (bradycardia)
reduced reflexes
constipation
increase in cholesterol
increase, sometimes vice versa decrease in pressure
enlargement of the tongue
lowered voice, hoarseness
snoring during sleep
Menstrual irregularities
weight gain.

Thyroid nodes

Nodules are a common pathology of the thyroid gland. Their signs can be:

Neck pressure feeling
Difficulty swallowing
Feeling of induration in the anterior region of the neck
external enlargement of the thyroid gland

Not all nodes are a disease, but with such signs, an ultrasound of the thyroid gland is necessary. Small nodes may not manifest themselves in any way, therefore it is recommended to do an ultrasound scan for all people once every few years.If large nodes are found, some signs on ultrasound, a fine-needle aspiration biopsy of the node is performed under ultrasound control. It is also necessary to determine calcitonin, as a tumor marker, in order to exclude the oncological process.

Thus, the general condition of the thyroid gland can be checked by two indicators: TSH and ultrasound. If these indicators show deviations from the norm, then it is necessary to check the levels of the hormones T3 and T4, as well as calcitonin.

Harmony begins where there is a fast and efficient metabolism.The thyroid gland is responsible for the quality of metabolism in the body, therefore it is so important to monitor the state of this small but so important organ.

The author of the article is Alexander Vladimirovich Lynnik, an endocrinologist at the Positivmed Medical Center.

You can find out more about the direction of endocrinology in our center here. Do not forget that our body is very fragile – sometimes serious pathologies arise without obvious symptoms. The specialists of our center recommend that all patients undergo an examination every few years to determine the general condition of the endocrine system.

You can make an appointment on our website, as well as by phone: 8 (812) 67-97-202

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Hormone with magical properties – Science – Kommersant

Regulation of sleep and fat metabolism, normalization of blood pressure, counteracting stress – all this and much more is considered the area of responsibility of the hormone melatonin.How they found it, how they found out its functions and what to do if melatonin is not enough – in this material.

“Beauty is a queen who reigns for a very short time,” Socrates said, and only now, more than 2000 years later, can we finally object to him.

Back in 1953, Aaron B. Lerner, a dermatologist from the United States who was looking for a cure for vitiligo, discovered a fairly old article from 1917 in a scientific journal. The article was about the fact that crushed epiphyses of cows, placed in a jar with tadpoles, within 30 minutes causes discoloration of their skin.Lerner and his colleagues processed 250,000 cow pineal glands and isolated a substance he called melatonin. This substance caused discoloration of the frog’s skin when applied to the skin. In 1958, Lerner established the structure of melatonin.

Here is the story of the discovery in just a few short sentences, when in reality it was years of hard work. After all, the content of melatonin in the pineal gland is negligible. And the legend associated with the name was born. As a reward for the scientific feat of processing 250 thousand.pineal glands, the substance received the name “melatonin” (from the Greek. melas – black, tosos – labor).

Although there is another, but less romantic version about the consonance of the name with melanin – a substance responsible for skin color.

Lerner’s discovery turned out to be more important than the scientist himself assumed. Ten years later, thanks to the studies of the biochemist Julius Axelrod, it was found that the pineal gland and its hormone melatonin are most directly related to the regulation of biological rhythms. Since then, an unprecedented “epiphyseal boom” has begun and continues to this day, literally overwhelming modern science.

The second wave began in 1974. This year is considered the beginning of the era of the study of extrapineal (extraepiphyseal) melatonin, since it was in this year that Russian scientists Natan Raikhlin and Igor Kvetny discovered melatonin in the mucous membrane of the human appendix. Later, the fact of extrapineal production of this indole hormone was proved.

It’s all about the “magic bubble”

Melatonin (N-acetyl-5-methoxytryptamine) is now known to be a 5-methoxy-N-acetylated derivative of serotonin.The main site of melatonin synthesis is the “magic bubble” – the pineal gland – a neuroendocrine organ of humans and mammals found in all vertebrates. In cold-blooded vertebrates and birds, the pineal gland plays the already well-known role of the “third eye”, supplying the body of these animals with information about daily and seasonal illumination. And in mammals and humans, the upper cerebral appendage, “buried” under the overgrown hemispheres and a powerful skull, lost direct afferent and efferent connections with the brain and turned into an endocrine gland.

As a result, the attention of world science to the pineal gland was attracted relatively recently. Only with the discovery of melatonin did this organ interest serious researchers. Prior to that, the pineal gland, the size of a pea, through the fault of evolutionary morphologists, was considered almost a “rudimentary third eye”, moreover, it had lost its connection with the rest of the brain, and therefore did not attract the attention of scientists. “It (the pineal gland) is devoid of any physiological significance and is a rudiment, which is already a teratoid formation in its variegated morphological composition,” wrote the famous pathophysiologist Alexander Bogomolets in his 1927 work “Endocrinology Crisis”.

Meanwhile, mankind has known the pineal gland for more than 2000 years, and in the past, oddly enough, despite its extremely small size, it was treated very respectfully. The ancient Indian philosophers considered the pineal gland to be the organ of reflections on the reincarnation of the soul and telepathy, the ancient Greeks took the pineal gland for a valve that regulates the amount of soul, or a structure necessary to establish mental balance.

It is believed that the pineal gland was first described by the Alexandrian physician Herophilus 300 BC.BC, and it got its name from Galen (II century AD), to whom the shape of the gland resembled a pine cone. In the 17th century, Rene Descartes attributed the role of the “seat of the soul” to the pineal gland and associated its functions with vision, which is very interesting in the light of modern knowledge. The Russian physician Yurovsky in 1695 presented a dissertation on the pineal gland, where he considered the pineal gland as a rudimentary appendage of the brain. This idea persisted throughout the 18th-19th centuries. Only at the very end of the 19th century, the German pediatrician Huebner described a boy who was distinguished by premature puberty, in whom a pineal gland tumor was found during postmortem autopsy.And at the beginning of the 20th century, the neurologist Marburg suggested that the pineal gland secretes some kind of substance that inhibits the functions of the hypothalamus and, as a result, the development of the reproductive system.

He’s the only one – the hormone melatonin

Melatonin is a unique hormone of photoperiodicity and is secreted by the pineal gland mainly at night, since its release is inhibited by impulses coming from the retina that reacts to light. The amount of its production is small – about 30 mcg per day.The concentration of the hormone, the minimum during the day (1-3 pg / ml), begins to increase two hours before the usual sleep time. Now it is clear that the appearance of “sand in the eyes” is caused by biological mechanisms, and not at all by the work of the fabulous Sand Man, or Ole Lukkoye, who pours magic sand into the eyes of children so that they fall asleep.

At night, the concentration of melatonin in the blood is five to ten times higher and reaches its peak by two in the morning, then its amount decreases by seven in the morning and remains very low until the evening.The secretion is strictly subordinate to the circadian rhythm, and about 70% of melatonin is synthesized at night.

This is why this hormone has been invisible for such a long time! Indeed, it is simply impossible to detect it in the blood in the light. Blood sampling for the determination of the concentration of melatonin in serum should be carried out in complete darkness with a sleeping patient under red light and at two in the morning.

There is also seasonal variation in melatonin synthesis. The level of melatonin in the blood in humans is minimal in the period from May to July, that is, during the period of maximum daylight hours and illumination.In the same months, the maximum value reaches the amplitude between the minimum (daytime) and maximum (nighttime) levels of melatonin during the day. Apparently, this is the reason for seasonal changes in the general hormonal activity and emotional state of a person – for example, seasonal depressions.

Melatonin production decreases with age. Moreover, the peak in nighttime serum melatonin levels is less pronounced in old age.

In the first three to six months of life, infants practically do not produce their own melatonin; the child receives this hormone with mother’s milk.It is clear that melatonin is not present in even a very adapted infant formula, but it strongly influences harmonious and rapid growth in the first year of a child’s life. Therefore, it is so important that both the child and the mother sleep in the dark, because it depends on whether the right amount of melatonin gets into the child’s body and whether the pineal gland starts functioning on time. In humans, the pineal gland reaches its maximum development by six to seven years of life, and the maximum total secretion of melatonin is observed exactly at the same age, after which, despite the continued functioning, age-related involution of the pineal gland begins.By the period of puberty, the size of the pineal gland usually decreases and the concentration of melatonin decreases several times.

The “melatonin curve” is quite individual for each person and differs from person to person. Moreover, a significant decrease in the production of melatonin in the majority begins after 40 years. With age, the deposition of phosphate and carbonate salts in the form of layered balls, the so-called “brain sand”, increases in the tissues of the pineal gland. As a result, the pineal gland really looks like a spruce cone, from which it got its name – the pineal gland.At that time, centenarians had a fairly high level of this melatonin in the blood.

Another source of melatonin is the cells of the APUD system. The melatonin they produce acts directly at the site of formation. Whether this pathway of hormone synthesis is photodependent or not is still to be clarified. Extrapineal melatonin is produced in the retina, mucous membrane and submucosa of the gastrointestinal tract, cerebellum, lungs, liver, kidneys, adrenal glands, thymus, thyroid and pancreas, gallbladder, inner ear, ovaries, carotid body, placenta, endometrium, and gland, reduced in humans and many mammals.In addition, melatonin is found in eosinophils, platelets, killer cells, histiocytes, and endothelial cells. Interestingly, this substance has been found even in unicellular organisms and plants.

The synthesis of melatonin by the pineal gland is regulated by photons of light and increases in the dark. From tryptophan, by the action of an enzyme, 5-hydroxytryptophan is formed, from which serotonin is formed with the help of another enzyme. If at this moment the light is on, then the synthesis stops at this stage.And the body gets serotonin. And it happens like this: when light acts on the retina, an electrical impulse is sent to the suprachiasmatic nucleus of the brain, then through noradrenergic connections, synthesis is inhibited at this stage, as well as inhibition of melatonin secretion by the pineal gland. If this reaction occurs in the dark, then N-acetylation of serotonin then occurs, then O-methylation, as a result of which melatonin is formed. Thus, light is the magic wand in this transformation.From tryptophan (an essential amino acid), as at the behest of a magic wand – light – either the hormone of darkness, melatonin, or the hormone of the day, serotonin, can be formed.

The level of the hormone in the blood depends not only on age, but also on the quality of sleep, ambient temperature, exposure to electromagnetic fields, changes in the phases of the menstrual cycle, gender (women have 25% higher melatonin levels than men).

Most of the plasma melatonin (about 70%) is associated with the albumin fraction.Its half-life in the human body is 30-50 minutes. Melatonin is biotransformed in the liver (about 90%) by the system of enzymes associated with the P-450 protein, and then excreted from the body. The secretion of the hormone occurs through the kidneys. At the same time, only traces of unchanged melatonin were found in the urine. Hydroxylated metabolites of melatonin are excreted in the urine mainly in the form of sulfates, and to a lesser extent in the form of glucuronides. The excretion of the main melatonin metabolite 6-SOMT by the kidneys corresponds to the concentration of melatonin in the blood serum, by the level of excretion of which in the urine one can indirectly judge the total synthesis of melatonin in the human body.

A small-sized melatonin molecule is highly lipophilic, overcomes all tissue barriers, freely passes through cell membranes. Melatonin can affect intracellular processes, bypassing the system of receptors and signaling molecules, interacting with nuclear (retinoid) and membrane receptors.

For the first time, receptors for melatonin were found in the brain and caudate artery of rats. To date, two types of receptors, MEL-1 and MEL-2, have been isolated and cloned in mammals.MEL-1 receptors are located in the vascular endothelium, heart, brain, kidneys, retina and peripheral tissues and are divided into MEL-1A (in the anterior pituitary gland, suprachiasmatic nuclei of the hypothalamus and peripheral organs), MEL-1B (in the brain, retina, lungs) and MEL-1C (their role is not yet clear). MEL-2 receptors are less studied and are found in the periphery. The number of receptors depends on age, the physiological state of the body and the circadian rhythm of melatonin, and their sensitivity depends on the time of day.With age, the number of receptors decreases. The largest number of receptors in the brain is found in the anterior part of the pituitary gland and in the suprachiasmatic nuclei.

Run your dream

Why is melatonin needed? The answer is: to manage the dream! A dream to stay active, beautiful and young as long as possible.

Melatonin has so many useful and necessary properties that our body is not only unable to refuse it, but also needs it every day. Melatonin eliminates insomnia, preserves the natural structure of sleep; adapts the body to a change in climatic and geographical zones and a rapid change in time zones; slows down the aging of the reproductive system; normalizes circadian and circanual rhythms of the body; optimizes cognitive activity of the brain and prevents its impairments, improves perception processes; weakens anxious behavior and a sense of fear, has an antidepressant and anti-stress effect; has a stimulating effect on fat-carbohydrate metabolism; reduces energy expenditure of the myocardium, inhibits platelet aggregation, normalizes blood pressure; normalizes motility, rhythm and secretory activity of the stomach; has an immunomodulatory and antioxidant effect; slows down the aging process; regulates the endocrine system (thyroid, pancreas, sex glands).Perhaps this is not a complete list of the “magic” properties of melatonin, scientists are still continuing to study the “invisibility”.

Let’s change life for the better

If the pineal gland is called the “orchestra conductor” of the endocrine system and the biological clock of the body, and melatonin is called the “pendulum of the biological clock”, then there is something to think about.

It is known for certain that living in the North, shift work, Jet lag (transmeridian flights), constant lighting (light at night, or the so-called light pollution), insomnia and social Jet lag (the difference in the rhythm of sleep-wakefulness during the week) are exactly the reasons that lead to a lack of melatonin.

To somehow remedy the matter, artificial melatonin appeared – a chemical analogue of natural melatonin, synthesized from amino acids of plant origin. Why is artificial melatonin plant-based? It’s simple: no need to scoff at hamsters, guinea pigs or cows, extracting the necessary hormone from their pineal gland. There is no need to spend finances on a thorough purification of the biogenic preparation (from allergens, viruses and pyrogenic proteins). And what about the prions now known to everyone? It is impossible to get rid of them at all.Therefore, semi-herbal melatonin is much safer and cheaper.

Exogenous melatonin has been studied in sufficient detail as a pharmacological agent. It is a low-toxic compound with LD50 for laboratory animals above 800 mg / kg. In humans, administration of melatonin for one month up to 6 g daily did not cause side effects. Taking physiological doses of the drug causes a mild hypnotic effect without changing the structure of sleep. The parenterally administered hormone easily penetrates the BBB, rapidly accumulates in the cerebrospinal fluid and brain tissue.The maximum level of melatonin was found in rats one hour later in the right parts of the brain. Melatonin preparations appeared for the first time in the USA in 1993. And today, in different countries, they act either as drugs or as a biological food supplement.

Various dosage forms of melatonin are sold worldwide, including immediate and sustained release forms. Dosages of melatonin are also different – from 0.3 mg to 5 mg. The most common dosage is 3 mg. But at present, it is considered to be quite large, since it exceeds physiological norms several times.Therefore, 1/4 or 1/2 of such a pill is suitable for an ordinary person.

The most commonly used dosage form of melatonin is tablets. But at present, in addition to the usual melatonin in tablets with different dosages, combined preparations are produced. Melatonin can be combined with vitamin B6 (pyridoxine). As you know, this is the only vitamin that is able to penetrate the blood-brain barrier, and it promotes the conversion of glutamic acid into GABA (which is an inhibitory mediator in the central nervous system).There are also combinations with zinc and selenium. A lot of sports nutrition with melatonin is produced. In addition to the tabulated, there is melatonin in capsules, in mixtures, in the form of a nasal spray. Cosmetics for skin care with melatonin (lotions, creams, gels) have appeared, which have an antioxidant, moisturizing and regenerating effect. When applied, there is a reduction in superficial wrinkles, restoration of skin elasticity and tone. Regular use, studies have shown, prevents premature aging of the epidermis.The photoprotective effect of melatonin when applied externally was also noted (it absorbs 27.17% of UV-B rays and 12.29% of UV-A rays). It can also be used in complex cosmetic programs, such as contouring, mesotherapy, botulinum toxin injections – to prolong the action of the main procedure; in pre- and post-peeling care. In aesthetic surgery and permanent make-up, melatonin promotes rapid recovery, prevents the development of secondary infections, and increases local immunity.

A prolonged-release melatonin with a duration of eight hours appeared on the pharmaceutical market. Such a medicine is indicated only for people over 55 years old, and this is understandable: since all hormones work according to the principle of negative feedback, such a long-term presence of exogenous melatonin in the body is shown only when there is an age-related decrease in the level of this hormone.

Currently, drugs are actively being developed that affect melatonin receptors, which are analogs of melatonin, but differ from it in chemical structure and sensitivity to MT1 and MT2 receptors.For example, the developed and already introduced drug agomelatine is an antidepressant. Agomelatine is a unique drug because it acts as a selective agonist of MT1 and MT2 receptors and an antagonist of serotonin (5-HT2B and 5-HT2C) receptors. This drug is registered in Russia. Two more drugs – ramelteon and tasimelteon – are positioned as new drugs for the treatment of insomnia and are selective agonists of melatonin receptors (MT1 and MT2). Tazimelteon is approved by the US Food and Drug Administration for use in completely blind patients with diurnal sleep disorder syndrome.

Genuine Beauty Secrets

How to determine if there is a lack of melatonin in the body and whether additional intake is necessary? The most reliable way is to measure its content. The currently developed very sensitive (from 0.5 pg / ml) methods for the determination of this hormone not only in blood plasma, but also in urine and saliva, make its use quite possible and justified. Doses, time and course of administration are decided in each case individually, taking into account the shape of the melatonin curve.There are already specially developed schemes for the use of this drug, depending on the type of disease, gender and age.

If sleep becomes more shallow and restless, if an inappropriate lifestyle disrupts the sleep-wake cycle, if sleep problems occur, the likely cause is low melatonin secretion. In this case, there are two possible ways to solve the problem: sleeping in absolute darkness for the full production of its own melatonin, or taking exogenous melatonin with an age-related decrease in the production of this hormone.Compliance with the daily routine, sufficient light exposure in the daytime, bedtime before midnight, prolonged sleep (seven to eight hours) in complete darkness (blackout curtains on the windows; switched off TV, computer, night light; use of a blindfold for sleep), consumption of foods rich in tryptophan (bananas, turkey, chicken, cheese, nuts, seeds) – these are fairly simple rules that allow you to maintain the secretion of melatonin at the proper physiological level.

If possible, it is advisable to stop taking drugs that lower melatonin levels at night (non-steroidal anti-inflammatory drugs, b-blockers, calcium channel blockers, inhibitors of the sympathetic nervous system, tranquilizers), also reduce melatonin levels, caffeine, nicotine and alcohol.Take vitamin and mineral complexes with vitamins B3 and B6, calcium and magnesium in the spring and summer, which increase the production of melatonin.

For those who have not been helped by all of the above measures, doctors recommend melatonin preparations, especially during the white nights season, with shift work or changing time zones. Undoubtedly, further extended clinical trials of the use of melatonin or other drugs that stimulate melatonin receptors or the production of endogenous melatonin are needed to expand the indications, to develop optimal treatment regimens depending on the cause of the deficiency of this hormone.

Irina Vinogradova, Doctor of Medical Sciences, Professor, Head of the Department of Pharmacology, Organization and Economics of Pharmacy, Petrozavodsk State University, Medical Institute

90,000 Pituitary gland. Location, structure, main hormones of the pituitary gland.

Pituitary gland (cerebral appendage) – endocrine gland, which is located in the so-called. Turkish saddle at the base of the skull.

Pituitary gland. Location.

Location of the pituitary gland in the skull

Topographically, it is located approximately in the center of the head.

The weight of the pituitary gland is only about 1 gram, and the dimensions do not exceed 14-15 mm.

The pituitary gland has an oval shape and is located in an isolated bone bed (Turkish saddle), which also has an oval shape. The pituitary gland is surrounded by bony formations on three sides – in front, behind and below. On the sides of the pituitary gland are the cavernous sinuses – hollow cavities consisting of sheets of the dura mater, inside which such important vessels as the carotid arteries and nerves pass, most of which control the movement of the eyeballs.From above, the cavity of the sella turcica is also limited by the fibrous layer of the dura mater – the diaphragm, which has an opening in the center, through which the pituitary gland is connected by means of the leg to one of the parts of the brain – the hypothalamus. Figuratively speaking, the pituitary gland hangs down on a leg (stem) like a cherry on a handle.

As a rule, the pituitary gland occupies the entire volume of the sella turcica, however, there are various options when it occupies only half of it, or vice versa, the pituitary gland increases in size, even slightly beyond the upper boundaries of the sella turcica.

Pituitary gland. Structure.

The structure of the pituitary gland

The cerebral appendage consists of two lobes – anterior (adenohypophysis, glandular lobe) and posterior (neurohypophysis), which have different origins: the anterior lobe is formed from the protrusion of the primary oral cavity (Rathke pocket), and the posterior one from the protrusion of the bottom of the 3rd ventricle of the brain during embryonic development. Also, the anterior and posterior lobes of the pituitary gland differ in functions: the adenohypophysis independently produces hormones, and the neurohypophysis only accumulates and activates them.

The adenohypophysis is the largest part of the pituitary gland and accounts for about 75% of its total mass. It consists of glandular cells, which, like a honeycomb in a hive, are separated by numerous trabecular strands.

Glandular cells are divided into 5 main types according to the type of hormonal substances they produce: somatotrophs, lactotrophs, corticotrophs, thyrotrophs, gonadotrophs.

Somatotrophs or cells producing somatotropic hormone (growth hormone, STH), the main hormone responsible for the growth of the body, make up about half of the entire cellular composition of the adenohypophysis and are located mainly on the sides of the lobe.

The pituitary gland is normal

With the development of a tumor from these cells, due to an increase in the secretory function of these cells and an increased production of STH, a disease called acromegaly develops.

Lactotrophs, or cells that produce prolactin, a hormone responsible for the formation of milk in the mammary glands, make up about 1/5 of all cells of the anterior pituitary gland and are located in the posterolateral regions. During pregnancy, their number increases almost 2 times, which is manifested by an increase in the size of the cerebral appendage.In addition to pregnancy, their increase can cause a decrease in the function of the thyroid gland – hypothyroidism, taking hormonal drugs containing estrogens. With an increase in the function of lactotrophs or the development of a tumor from these cells, a person develops hyperprolactinemia.

Corticotrophs are cells that synthesize various biological active substances, one of which is adrenocorticotropic hormone (ACTH), a hormone that regulates the secretion of a number of hormones by the adrenal glands, one of the main ones being cortisol.They, like lactotrophs, make up about 20% of all cells of the adenohypophysis. With their hyperplasia or the development of a tumor, a person develops hypercorticism, called Itsenko-Cushing’s disease.

Thyrotrophs, or cells that secrete thyroid-stimulating hormone (TSH), a hormone responsible for the growth of the thyroid gland and the regulation of its secretion of hormones called T3 and T4. They make up only 5% of the cellular composition of the adenohypophysis. They are located mainly in the anterior parts of the adenohypophysis. With the development of hypothyroidism, they increase in size (hyperplastic), their number increases, which can lead to the formation of a tumor – thyrotropinoma.

Gonadotrophs, or cells that secrete sex hormones (gonadotropins), make up about 10-15% of the cellular composition of the adenohypophysis. They are localized evenly along the anterior lobe of the pituitary gland, but mainly in the lateral regions. These cells produce two types of hormones – follicle-stimulating hormone (FSH) – responsible for stimulating ovulation in women and sperm production in men, and luteinizing hormone (LH) – stimulating ovulation in women and testosterone production in men.

These cells can also grow in size during hypogonadism.

In addition to hormonally active cells in the anterior lobe of the pituitary gland there are also cells that are not stained with special methods that determine the secretory activity of cells. These are the so-called null cells, which serve as a source for the formation of non-functioning pituitary adenomas.

Their activity is not fully understood, however, it is believed that they can produce some types of hormones in low concentration or in an inactive form.

In the anterior lobe of the pituitary gland, 6 hormones are produced, which can be divided into 3 groups:
1) protein hormones related to somatomammotropins – STH and prolactin;
2) glycoproteins – FSH, LH and TSH;
3) hormones that are derivatives of POMC – ACTH, lipotropins, melanostimulating hormone (MSH), endorphins and related to polypeptides.

The average lobe of the pituitary gland in humans is practically absent and does not take part in hormone formation.

Two types of hormones produced in the hypothalamus accumulate in the posterior lobe of the pituitary gland – antidiuretic hormone (controls the feeling of thirst and the amount of urine excreted by the kidneys) and oxytocin (stimulates uterine contraction in women), which enter it along the axons of neurons located in the hypothalamic nuclei, where synthesis of these hormones is carried out. In addition to the function of depositing, the neurohypophysis carries out their kind of activation, after which hormones in an active form are released into the blood.

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90,000 Goiter (struma), Multinodular, nodular or diffuse goiter

Goiter (struma), multinodular, nodular or diffuse goiter

Goiter – persistent enlargement of the thyroid gland, due to the growth of benign tumors, which is not associated with malignant growth, inflammation.

The thyroid gland can increase evenly (diffuse goiter) or limited seals can form in it – nodular goiter.If the function of the gland is reduced, hypothyroid goiter develops, if it is increased, toxic goiter.

The goiter is usually located on the front of the neck, less often behind the sternum, at the root of the tongue. The development of goiter in atypical places can squeeze nearby tissues and vessels (aorta, carotid artery, jugular vein), interfere with food swallowing, change the timbre of the voice, in patients with bronchial asthma it can provoke asthma attacks.

Causes of occurrence

The world’s most widespread endemic goiter, which occurs when there is a lack of iodine in food.Other causes may be hypothyroidism, the use of strumogenic products, congenital disorders in the synthesis of thyroid hormones, side effects of drugs, diffuse toxic goiter, thyroiditis, hyperthyroidism, and thyroid cancer.

Symptoms

Goiter not associated with endocrine dysfunction, as a rule, manifests itself only by enlargement and deformation of the anterior surface of the neck. A large goiter can compress the surrounding anatomical structures, making it difficult to swallow and breathe.

Goiter, combined with thyroid dysfunction, is accompanied by a characteristic symptom complex of hypothyroidism or thyrotoxicosis.

Symptoms of hypothyroidism (insufficient production of thyroid hormones): dry and pale skin, hair loss, brittle nails, decreased appetite, thinning eyebrows, weight gain. With a pronounced pathological process, speech slows down, constant drowsiness appears, memory deteriorates, and the menstrual cycle is disrupted.

Thyrotoxicosis (increased production of thyroid hormones) is manifested by insomnia, irritability, general weakness, palpitations, weight loss due to increased appetite, high blood pressure, excessive sweating, tremors in the hands (tremors).

Diagnostics

The primary diagnosis of the disease is palpation of the thyroid gland.

Standard examination – ultrasound examination of the thyroid gland to determine the exact size of the thyroid gland, the presence of formations in it. If a formation with a diameter of 1 cm or more is detected, a fine-needle aspiration biopsy (TAPB) is prescribed. With a smaller node, this procedure is performed if a malignant process is suspected.

With large goiter and retrosternal location, there is a risk of airway compression.In such situations, an x-ray of the chest, esophagus is necessary.

For a more detailed study of the retrosternal goiter, they resort to CT or MRI (magnetic resonance imaging).

Types of disease

Depending on the cause and mechanism of development, there are:

Endemic goiter – in geographic regions endemic for goiter;

Sporadic goiter – in non-endemic goiter areas.

By structure:

Nodular goiter;

Diffuse goiter;

Mixed goiter (diffuse nodular).

By location:

Usually located;

Ring;

Partially retrosternal;

Dystopic goiter from embryonic anlages (accessory lobe of the thyroid gland, root of the tongue).

On functional grounds distinguish:

Hypothyroidism – reduced production of thyroid hormones.

Euthyroidism – the production of hormones of the gland is not impaired.

Thyrotoxicosis or hyperthyroidism – production of increased amounts of thyroid hormones.

By the degree of enlargement of the thyroid gland (WHO classification):

Grade 0 – no goiter.

Grade I – the goiter is palpable, but not visualized in the normal position of the neck.

Grade II – the goiter is palpable and visible to the eye.

Patient actions

At the first signs of the disease, you should consult an endocrinologist.

Treatment

In most cases, the disease requires special treatment.Patients need to periodically visit an endocrinologist to monitor the course of the disease.

In case of a large goiter, the presence of compression syndrome, rapid growth of nodes, visualization of a tumor on the neck, it is necessary to carry out surgical methods of treatment, consisting in total removal of the thyroid gland – thyroidectomy, or removal of the lobe of the thyroid gland – hemithyroidectomy.

For small thyroid nodules, minimally invasive methods of treatment are possible: LIT (laser interstitial thermal ablation), sclerotherapy or a combination of these methods, which will avoid disabling surgical treatment.

The department also performs organ-preserving operations on the thyroid gland, a combination of hemithyroidectomy and LIT, resection of the thyroid gland according to indications.

Complications

The complications of goiter include mechanical compression of the enlarged thyroid gland of adjacent organs, malignant degeneration of the goiter, hemorrhages in the goiter, inflammatory processes (strumites).

Prevention

Prevention of goiter is reduced to increasing the use of iodized foods in the diet.

90,000 MRI of the pituitary gland and surrounding structures in the MEDSI clinic

The endocrine system includes special glands, the cells of which are secreted into the internal environment of the body, i.e. into the blood or lymph, chemical regulators called hormones. The concept of “hormone” (from the Greek hormaino – inspire, set in motion) was proposed by Beilis and Starling (1905). Currently, hormones are substances that are formed in glandular cells, released into the blood or lymph and regulate the metabolism and development of the body.

Hormones share the following common biological characteristics:

Distance of action, i.e. they regulate the exchange and function of effector cells at a distance of
High biological activity – very small amounts are enough, sometimes a dozen micrograms, to keep the body alive

The glands that secrete hormones are sometimes divided into central, anatomically associated with parts of the central nervous system, and peripheral.

The central glands include the hypothalamus, pituitary gland, pineal gland; to the peripheral – the thyroid gland, adrenal glands, sex glands, placenta, thymus.

The pituitary gland is located at the base of the brain in the cavity of the sella turcica and consists of two lobes: anterior (adenohypophysis) and posterior (neurohypophysis). The pituitary gland is a small gland that weighs no more than 1 gram. The normal height of the pituitary gland is 3-8 mm and the width is 10-17 mm. Its upper surface is usually flat or somewhat concave, less often convex.The convex surface of the pituitary gland is more common in young women.

The pituitary gland secretes a large number of hormones involved in the regulation of various biological processes and physiological functions. In the anterior lobe of the pituitary gland (adenohypophysis), the so-called tropic hormones are synthesized, stimulating the synthesis and secretion of hormones from other endocrine glands or influencing metabolic reactions in other target tissues. The posterior lobe of the pituitary gland, or the neurohypophysis, secretes hormones that mainly regulate water balance and smooth muscle tone.

Adenohypophysis produces hormones:

Growth hormone (somatotropic hormone) – stimulates the growth of the skeleton and soft tissues; participates in the regulation of energy and mineral metabolism
Thyrotropin – stimulates the synthesis of iodothyronines
Prolactin – stimulates lactation

Luteinizing hormone – induces ovulation in women, androgen synthesis in men

Follicle-stimulating hormone – stimulates the growth of follicles in women, in men – spermatogenesis
Corticotropin (adrenocorticotropic hormone) – stimulates the growth of the adrenal glands and the synthesis of corticosteroids
B-lipotropin – stimulates lipolysis
Melatropin – synthesis of skin melanins, iris

Although the pituitary gland is separated by a distance of about a meter from the gonads, but it is he who controls their functions, causes the maturation of follicles in the ovaries, ovulation, the secretion of female sex hormones, affects the uterus.It also affects the male genital organs, adrenal glands, and the thyroid gland. In other words: the pituitary gland has no pronounced sexual specificity, therefore, it is asexual. Diseases such as obesity, a number of mental disorders, infertility depend on its improper activity. In other words, he, as a conductor, affects the endocrine “sound” of the body. Therefore, the statement of the Canadian physiologist G. Selye that the pituitary gland is a kind of “endocrine brain” should be recognized as absolutely accurate.

The pituitary gland is closely connected with the hypothalamus – the place of contact between nervous and hormonal reactions.Their neighborhood is not only territorial, but also functionally important.

Prolactin is synthesized by lactotrophic cells of the anterior pituitary gland in the form of a prohormone. The number of these cells increases dramatically during pregnancy under the influence of estrogens. Like most hormones, prolactin is secreted into the blood sporadically at intervals of 30-90 minutes. The maximum secretion is noted 6-8 hours after the onset of sleep. The concentration of prolactin in the blood plasma of women is 8-10 ng / ml, and in men – 5-8 ng / ml.

There are many different diseases associated with excessive or insufficient release of various pituitary hormones.

Typical manifestations of such diseases are dwarfism (the modern name is growth hormone deficiency) and gigantism. These diseases are associated with a violation of the production of growth hormone – a substance that regulates the growth rate of a person in childhood. Examples of other diseases of the pituitary gland are acromegaly, Itsenko-Cushing’s disease, hyperprolactinemia (increased prolactin levels), diabetes insipidus, as well as abnormalities in the work of other endocrine glands due to impaired control by the pituitary gland.

Various tumors of the pituitary gland, hypothalamus and surrounding structures can lead to dysfunction of the pituitary gland. Tumor diseases of the pituitary gland in most cases are adenomas, i.e. benign tumors. The reasons for the formation and growth of pituitary adenomas are unclear. Predisposing factors are various neuroinfections, brain injuries, radiation injuries. Adenomas can be hormone-producing and hormone-producing. The hormonally active formations of the pituitary gland are of clinical importance.The most common problem is prolactinoma. If the size of the tumor does not exceed 10 mm, then it is called a microadenoma. If the formation is large, it is called a macroadenoma. If the size of the adenomas is large, then it can squeeze the brain tissue, causing visual and other neurological disorders.

The most informative method in detecting lesions of the pituitary gland is MRI of the pituitary gland and its surrounding structures (chiasmatic – sellar region). Since the size of the pituitary gland is small, in order to assess its changes, which may not affect the entire pituitary gland, but only part of it, it is necessary to obtain images of the minimum thickness and high resolution.The optimum cutting thickness is 2-3 mm. Therefore, MRI of the pituitary gland is performed as a separate procedure, according to a special protocol that differs from MRI of the brain. Compared to common 1.5 Tesla tomographs, the higher magnetic field voltage of 3 Tesla, even with the smallest slice thickness, allows high-resolution images to be obtained, which makes it possible to recognize the causes of diseases that are associated with minimally noticeable changes. One of the most common reasons for conducting an MRI of the pituitary gland is suspicion of the presence of a microadenoma, which can be manifested by an increase in the level of prolactin in the blood.In this case, it is better to do an MRI of the pituitary gland with the introduction of a contrast agent. In some cases, microadenoma can be seen only in post-contrast images. In the event that the formations reach large sizes, contrasting allows you to better see the contours of the formation, its relationship with the surrounding structures (including with nearby optic nerves), and evaluate its structure. The amount of contrast agent injected depends on the weight of the patient.

Polymorphisms of reproductive hormone receptor genes

The biological effect of any hormone on the target cell is carried out through the hormone-receptor complex, that is, for a cellular response to occur, it is necessary for the hormone to enter into a connection with the receptor.Despite the variety of hormones and receptors in the human body, all receptors are divided into 2 types – membrane and intracellular. And the functional characteristics are expressed either in the ability to bind to the hormone, or in the impaired signal conduction function.

Receptors of gonadotropic hormones of the hypothalamus and pituitary gland are receptors of the cell membrane and are G-protein. Like all proteins in the body, they are encoded by specific genes. Polymorphisms (expressed in the replacement of single nucleotide sequences in DNA) affecting the coding parts of these genes often lead to amino acid substitutions in the protein molecule and the appearance of receptor proteins with distorted functional properties.

The LHCGR gene encodes the luteinizing hormone (LH) receptor. LH receptors in a woman’s body are located on the theca-luteal cells of the ovary, the receptors are critical for the maintenance of theca, follicular maturation and ovulation. LHR-mediated signals play an important role in the ovarian response to exogenous FSH administration.

At least 300 LHCGR polymorphisms are known to have a significant effect on sexual development and fertility. Mutations in the LH receptor gene are of two types: receptor activating and inactivating.An activating mutation in boys causes premature sexual development, which can begin before the age of 1 year, with another mutation up to 4 years. In women, the phenotypic manifestation of activating mutations in the LH receptor gene was not observed.

Inactivating mutations (8 mutations) of the LH receptor gene cause impaired signal conduction when exposed to LH, or lead to a decrease in the ability of the receptor to bind to LH. Inactivating mutations determine a whole spectrum of clinical manifestations.The most severe are due to the homozygous carriage of these mutations. They appear during the period of male differentiation in embryogenesis. Male pseudohermaphroditism may form (testosterone synthesis by testicles is impaired due to hypoplasia of Leydig cells or their complete absence). With mild forms of pathology, in contrast to the classic version of male pseudohermaphroditism, hypogonadism is formed with severe hypoplasia of the external genital organs. And here the differential diagnosis with hypogonadism in men, caused by a mutation in another gene – in the gene of the β-subunit of LH, is very important.In women, homozygous carriage of mutant alleles of the LH receptor gene is accompanied by a slight change in the phenotype. But at the same time, primary amenorrhea and infertility can be noted.

GNRHR – the gene for the gonadotropin-releasing hormone receptor (GnRH, GNRH) is located on chromosome 14 (14q21.1). The study is important for the differential diagnosis of clinical forms such as idiopathic hypogonadotropic hypogonadism (IHH). The clinical picture of hypogonadotropic hypogonadism in men is characterized by decreased libido, lack of facial hair, rare pubic hair, and reduced testicular mass.Puberty begins at age 16. In women, primary amenorrhea and infertility are observed. The external genitals and mammary glands are normally developed.

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