هرمون

(تم التحويل من بهرمون)
Left: A hormone feedback loop in a female adult. (1) follicle-stimulating hormone, (2) luteinizing hormone, (3) progesterone, (4) estradiol. Right: auxin transport from leaves to roots in Arabidopsis thaliana
إپينفرين (أدرينالين), a catecholamine-type hormone

الهرمونات هى مركبات حيوية يتم تصنيعها في غدد ضمن الأجسام الحية لتقوم بوظائف حيوية مختلفة استقلابية وبنائية فهى مواد كيمائية معقدة للغاية تفرزها خلايا خاصة بكميات ضئيلة جدا حسب حاجة الجسم اليها وقد ينشط افرازها خلايا عصبية مثل افراز الهرمونات عند الخوف والغضب كما انها تهيئ حالة الجسم حسب البيئة الخارجية كما انها لها دور مهم في العمليات الحيوية التى يقوم بها الكائن الحى فكل هرومون لة دورة ومتخصص في عملة ونقص الهرومونات يؤدى إلى حالة مرضية وربما الموت ويفرز الهرمون في الدم مباشرة من خلال غدد خاصة تسمة بالغدد الصماء كما انة هناك نوع اخر من الهرومونات تفرز غدد قنوية مثل الغدد اللعابية الموجودة تحت اللسان وهنال نوع ثالث من الغدد يسمى بالغدد المشتركة والتى تفرز هرومونات في الدم مباشرة وهرومونات خارجية مثل غدة البنكرياس وتعتبر الغدة النخامية رئيسة الغدد التى تتحكم في جميع الغدد الاخرى وهى اصغر الغدد وتوجد في النصف السفلى من الرأس بينما اكبر الغدد هى الغدة الدرقية وتوجد في الرقبة ولها دور مهم في عملية ايض النشويات والتمثيل الغذائىوهى ايضا اكثر الغدد معرضة للتضخم نتيجة لنقص اليود في الطعام ولنبات هرومونات تسمى بالاوكسينات تساهم في نموه الخضرى.

Hormones are used to communicate between organs and tissues. In vertebrates, hormones are responsible for regulating a wide range of processes including both physiological processes and behavioral activities such as digestion, metabolism, respiration, sensory perception, sleep, excretion, lactation, stress induction, growth and development, movement, reproduction, and mood manipulation.[1][2][3] In plants, hormones modulate almost all aspects of development, from germination to senescence.[4]

Hormones affect distant cells by binding to specific receptor proteins in the target cell, resulting in a change in cell function. When a hormone binds to the receptor, it results in the activation of a signal transduction pathway that typically activates gene transcription, resulting in increased expression of target proteins. Hormones can also act in non-genomic pathways that synergize with genomic effects.[5] Water-soluble hormones (such as peptides and amines) generally act on the surface of target cells via second messengers. Lipid soluble hormones, (such as steroids) generally pass through the plasma membranes of target cells (both cytoplasmic and nuclear) to act within their nuclei. Brassinosteroids, a type of polyhydroxysteroids, are a sixth class of plant hormones and may be useful as an anticancer drug for endocrine-responsive tumors to cause apoptosis and limit plant growth. Despite being lipid soluble, they nevertheless attach to their receptor at the cell surface.[6]

In vertebrates, endocrine glands are specialized organs that secrete hormones into the endocrine signaling system. Hormone secretion occurs in response to specific biochemical signals and is often subject to negative feedback regulation. For instance, high blood sugar (serum glucose concentration) promotes insulin synthesis. Insulin then acts to reduce glucose levels and maintain homeostasis, leading to reduced insulin levels. Upon secretion, water-soluble hormones are readily transported through the circulatory system. Lipid-soluble hormones must bond to carrier plasma glycoproteins (e.g., thyroxine-binding globulin (TBG)) to form ligand-protein complexes. Some hormones, such as insulin and growth hormones, can be released into the bloodstream already fully active. Other hormones, called prohormones, must be activated in certain cells through a series of steps that are usually tightly controlled.[7] The endocrine system secretes hormones directly into the bloodstream, typically via fenestrated capillaries, whereas the exocrine system secretes its hormones indirectly using ducts. Hormones with paracrine function diffuse through the interstitial spaces to nearby target tissue.

Plants lack specialized organs for the secretion of hormones, although there is spatial distribution of hormone production. For example, the hormone auxin is produced mainly at the tips of young leaves and in the shoot apical meristem. The lack of specialised glands means that the main site of hormone production can change throughout the life of a plant, and the site of production is dependent on the plant's age and environment.[8]

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Introduction and overview

Hormone producing cells are found in the endocrine glands, such as the thyroid gland, ovaries, and testes.[9] Hormonal signaling involves the following steps:[10]

  1. Biosynthesis of a particular hormone in a particular tissue.
  2. Storage and secretion of the hormone.
  3. Transport of the hormone to the target cell(s).
  4. Recognition of the hormone by an associated cell membrane or intracellular receptor protein.
  5. Relay and amplification of the received hormonal signal via a signal transduction process: This then leads to a cellular response. The reaction of the target cells may then be recognized by the original hormone-producing cells, leading to a downregulation in hormone production. This is an example of a homeostatic negative feedback loop.
  6. Breakdown of the hormone.

Exocytosis and other methods of membrane transport are used to secrete hormones when the endocrine glands are signaled. The hierarchical model is an oversimplification of the hormonal signaling process. Cellular recipients of a particular hormonal signal may be one of several cell types that reside within a number of different tissues, as is the case for insulin, which triggers a diverse range of systemic physiological effects. Different tissue types may also respond differently to the same hormonal signal.[بحاجة لمصدر]


Discovery

Arnold Adolph Berthold (1849)

Arnold Adolph Berthold was a German physiologist and zoologist, who, in 1849, had a question about the function of the testes. He noticed in castrated roosters that they did not have the same sexual behaviors as roosters with their testes intact. He decided to run an experiment on male roosters to examine this phenomenon. He kept a group of roosters with their testes intact, and saw that they had normal sized wattles and combs (secondary sexual organs), a normal crow, and normal sexual and aggressive behaviors. He also had a group with their testes surgically removed, and noticed that their secondary sexual organs were decreased in size, had a weak crow, did not have sexual attraction towards females, and were not aggressive. He realized that this organ was essential for these behaviors, but he did not know how. To test this further, he removed one testis and placed it in the abdominal cavity. The roosters acted and had normal physical anatomy. He was able to see that location of the testes does not matter. He then wanted to see if it was a genetic factor that was involved in the testes that provided these functions. He transplanted a testis from another rooster to a rooster with one testis removed, and saw that they had normal behavior and physical anatomy as well. Berthold determined that the location or genetic factors of the testes do not matter in relation to sexual organs and behaviors, but that some chemical in the testes being secreted is causing this phenomenon. It was later identified that this factor was the hormone testosterone.[11][12]

Charles and Francis Darwin (1880)

Although known primarily for his work on the Theory of Evolution, Charles Darwin was also keenly interested in plants. Through the 1870s, he and his son Francis studied the movement of plants towards light. They were able to show that light is perceived at the tip of a young stem (the coleoptile), whereas the bending occurs lower down the stem. They proposed that a 'transmissible substance' communicated the direction of light from the tip down to the stem. The idea of a 'transmissible substance' was initially dismissed by other plant biologists, but their work later led to the discovery of the first plant hormone.[13] In the 1920s Dutch scientist Frits Warmolt Went and Russian scientist Nikolai Cholodny (working independently of each other) conclusively showed that asymmetric accumulation of a growth hormone was responsible for this bending. In 1933 this hormone was finally isolated by Kögl, Haagen-Smit and Erxleben and given the name 'auxin'.[13][14][15]

Oliver and Schäfer (1894)

British physician George Oliver and physiologist Edward Albert Schäfer, professor at University College London, collaborated on the physiological effects of adrenal extracts. They first published their findings in two reports in 1894, a full publication followed in 1895.[16][17] Though frequently falsely attributed to secretin, found in 1902 by Bayliss and Starling, Oliver and Schäfer's adrenal extract containing adrenaline, the substance causing the physiological changes, was the first hormone to be discovered. The term hormone would later be coined by Starling.[18]

Bayliss and Starling (1902)

William Bayliss and Ernest Starling, a physiologist and biologist, respectively, wanted to see if the nervous system had an impact on the digestive system. They knew that the pancreas was involved in the secretion of digestive fluids after the passage of food from the stomach to the intestines, which they believed to be due to the nervous system. They cut the nerves to the pancreas in an animal model and discovered that it was not nerve impulses that controlled secretion from the pancreas. It was determined that a factor secreted from the intestines into the bloodstream was stimulating the pancreas to secrete digestive fluids. This was named secretin: a hormone.

Types of signaling

Hormonal effects are dependent on where they are released, as they can be released in different manners.[19] Not all hormones are released from a cell and into the blood until it binds to a receptor on a target. The major types of hormone signaling are:

Signaling Types - Hormones
SN Types Description
1 Endocrine Acts on the target cells after being released into the bloodstream.
2 Paracrine Acts on the nearby cells and does not have to enter general circulation.
3 Autocrine Affects the cell types that secreted it and causes a biological effect.
4 Intracrine Acts intracellularly on the cells that synthesized it.

Chemical classes

As hormones are defined functionally, not structurally, they may have diverse chemical structures. Hormones occur in multicellular organisms (plants, animals, fungi, brown algae, and red algae). These compounds occur also in unicellular organisms, and may act as signaling molecules however there is no agreement that these molecules can be called hormones.[20][21]

Vertebrates

Hormone types in Vertebrates
SN Types Description
1 Proteins/

Peptides

Peptide hormones are made of a chain of amino acids that can range from just 3 to hundreds. Examples include oxytocin and insulin.[11] Their sequences are encoded in DNA and can be modified by alternative splicing and/or post-translational modification.[19] They are packed in vesicles and are hydrophilic, meaning that they are soluble in water. Due to their hydrophilicity, they can only bind to receptors on the membrane, as travelling through the membrane is unlikely. However, some hormones can bind to intracellular receptors through an intracrine mechanism.
2 Amino Acid

Derivatives

Amino acid hormones are derived from amino acids, most commonly Tyrosine. They are stored in vesicles. Examples include Melatonin and Thyroxine.
3 Steroids Steroid hormones are derived from cholesterol. Examples include the sex hormones estradiol and testosterone as well as the stress hormone cortisol.[22] Steroids contain four fused rings. They are lipophilic and hence can cross membranes to bind to intracellular nuclear receptors.
4 Eicosanoids Eicosanoids hormones are derived from lipids such as arachidonic acid, lipoxins, thromboxanes and prostaglandins. Examples include prostaglandin and thromboxane. These hormones are produced by cyclooxygenases and lipoxygenases. They are hydrophobic and act on membrane receptors.
5 Gases Ethylene and Nitric Oxide
Different types of hormones are secreted in the human body, with different biological roles and functions.

Invertebrates

Compared with vertebrates, insects and crustaceans possess a number of structurally unusual hormones such as the juvenile hormone, a sesquiterpenoid.[23]


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Plants

Examples include abscisic acid, auxin, cytokinin, ethylene, and gibberellin.[24]

Receptors

The left diagram shows a steroid (lipid) hormone (1) entering a cell and (2) binding to a receptor protein in the nucleus, causing (3) mRNA synthesis which is the first step of protein synthesis. The right side shows protein hormones (1) binding with receptors which (2) begins a transduction pathway. The transduction pathway ends (3) with transcription factors being activated in the nucleus, and protein synthesis beginning. In both diagrams, a is the hormone, b is the cell membrane, c is the cytoplasm, and d is the nucleus.

Most hormones initiate a cellular response by initially binding to either cell surface receptors or intracellular receptors. A cell may have several different receptors that recognize the same hormone but activate different signal transduction pathways, or a cell may have several different receptors that recognize different hormones and activate the same biochemical pathway.[25]

Receptors for most peptide as well as many eicosanoid hormones are embedded in the cell membrane as cell surface receptors, and the majority of these belong to the G protein-coupled receptor (GPCR) class of seven alpha helix transmembrane proteins. The interaction of hormone and receptor typically triggers a cascade of secondary effects within the cytoplasm of the cell, described as signal transduction, often involving phosphorylation or dephosphorylation of various other cytoplasmic proteins, changes in ion channel permeability, or increased concentrations of intracellular molecules that may act as secondary messengers (e.g., cyclic AMP). Some protein hormones also interact with intracellular receptors located in the cytoplasm or nucleus by an intracrine mechanism.[26][27]

For steroid or thyroid hormones, their receptors are located inside the cell within the cytoplasm of the target cell. These receptors belong to the nuclear receptor family of ligand-activated transcription factors. To bind their receptors, these hormones must first cross the cell membrane. They can do so because they are lipid-soluble. The combined hormone-receptor complex then moves across the nuclear membrane into the nucleus of the cell, where it binds to specific DNA sequences, regulating the expression of certain genes, and thereby increasing the levels of the proteins encoded by these genes.[28] However, it has been shown that not all steroid receptors are located inside the cell. Some are associated with the plasma membrane.[29]

Effects in humans

Hormones have the following effects on the body:[30]

A hormone may also regulate the production and release of other hormones. Hormone signals control the internal environment of the body through homeostasis.

Regulation

The rate of hormone biosynthesis and secretion is often regulated by a homeostatic negative feedback control mechanism. Such a mechanism depends on factors that influence the metabolism and excretion of hormones. Thus, higher hormone concentration alone cannot trigger the negative feedback mechanism. Negative feedback must be triggered by overproduction of an "effect" of the hormone.[31][32]

Blood glucose levels are maintained at a constant level in the body by a negative feedback mechanism. When the blood glucose level is too high, the pancreas secretes insulin and when the level is too low, the pancreas then secretes glucagon. The flat line shown represents the homeostatic set point. The sinusoidal line represents the blood glucose level.

Hormone secretion can be stimulated and inhibited by:

  • Other hormones (stimulating- or releasing -hormones)
  • Plasma concentrations of ions or nutrients, as well as binding globulins
  • Neurons and mental activity
  • Environmental changes, e.g., of light or temperature

One special group of hormones is the tropic hormones that stimulate the hormone production of other endocrine glands. For example, thyroid-stimulating hormone (TSH) causes growth and increased activity of another endocrine gland, the thyroid, which increases output of thyroid hormones.[33]

To release active hormones quickly into the circulation, hormone biosynthetic cells may produce and store biologically inactive hormones in the form of pre- or prohormones. These can then be quickly converted into their active hormone form in response to a particular stimulus.[33]

Eicosanoids are considered to act as local hormones. They are considered to be "local" because they possess specific effects on target cells close to their site of formation. They also have a rapid degradation cycle, making sure they do not reach distant sites within the body.[34]

Hormones are also regulated by receptor agonists. Hormones are ligands, which are any kinds of molecules that produce a signal by binding to a receptor site on a protein. Hormone effects can be inhibited, thus regulated, by competing ligands that bind to the same target receptor as the hormone in question. When a competing ligand is bound to the receptor site, the hormone is unable to bind to that site and is unable to elicit a response from the target cell. These competing ligands are called antagonists of the hormone.[35]

Therapeutic use

Many hormones and their structural and functional analogs are used as medication. The most commonly prescribed hormones are estrogens and progestogens (as methods of hormonal contraception and as HRT),[36] thyroxine (as levothyroxine, for hypothyroidism) and steroids (for autoimmune diseases and several respiratory disorders). Insulin is used by many diabetics. Local preparations for use in otolaryngology often contain pharmacologic equivalents of adrenaline, while steroid and vitamin D creams are used extensively in dermatological practice.[37]

A "pharmacologic dose" or "supraphysiological dose" of a hormone is a medical usage referring to an amount of a hormone far greater than naturally occurs in a healthy body. The effects of pharmacologic doses of hormones may be different from responses to naturally occurring amounts and may be therapeutically useful, though not without potentially adverse side effects. An example is the ability of pharmacologic doses of glucocorticoids to suppress inflammation.

Hormone-behavior interactions

At the neurological level, behavior can be inferred based on hormone concentration, which in turn are influenced by hormone-release patterns; the numbers and locations of hormone receptors; and the efficiency of hormone receptors for those involved in gene transcription. Hormone concentration does not incite behavior, as that would undermine other external stimuli; however, it influences the system by increasing the probability of a certain event to occur.[38]

Not only can hormones influence behavior, but also behavior and the environment can influence hormone concentration.[39] Thus, a feedback loop is formed, meaning behavior can affect hormone concentration, which in turn can affect behavior, which in turn can affect hormone concentration, and so on.[40] For example, hormone-behavior feedback loops are essential in providing constancy to episodic hormone secretion, as the behaviors affected by episodically secreted hormones directly prevent the continuous release of sad hormones.[41]

Three broad stages of reasoning may be used to determine if a specific hormone-behavior interaction is present within a system:[بحاجة لمصدر]

  • The frequency of occurrence of a hormonally dependent behavior should correspond to that of its hormonal source.
  • A hormonally dependent behavior is not expected if the hormonal source (or its types of action) is non-existent.
  • The reintroduction of a missing behaviorally dependent hormonal source (or its types of action) is expected to bring back the absent behavior.

Comparison with neurotransmitters

Though colloquially oftentimes used interchangeably, there are various clear distinctions between hormones and neurotransmitters:[42][43][35]

  • A hormone can perform functions over a larger spatial and temporal scale than can a neurotransmitter, which often acts in micrometer-scale distances.[44]
  • Hormonal signals can travel virtually anywhere in the circulatory system, whereas neural signals are restricted to pre-existing nerve tracts.[44]
  • Assuming the travel distance is equivalent, neural signals can be transmitted much more quickly (in the range of milliseconds) than can hormonal signals (in the range of seconds, minutes, or hours). Neural signals can be sent at speeds up to 100 meters per second.[45]
  • Neural signalling is an all-or-nothing (digital) action, whereas hormonal signalling is an action that can be continuously variable as it is dependent upon hormone concentration.

Neurohormones are a type of hormone that share a commonality with neurotransmitters.[46] They are produced by endocrine cells that receive input from neurons, or neuroendocrine cells.[46] Both classic hormones and neurohormones are secreted by endocrine tissue; however, neurohormones are the result of a combination between endocrine reflexes and neural reflexes, creating a neuroendocrine pathway.[35] While endocrine pathways produce chemical signals in the form of hormones, the neuroendocrine pathway involves the electrical signals of neurons.[35] In this pathway, the result of the electrical signal produced by a neuron is the release of a chemical, which is the neurohormone.[35] Finally, like a classic hormone, the neurohormone is released into the bloodstream to reach its target.[35]


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Binding proteins

Hormone transport and the involvement of binding proteins is an essential aspect when considering the function of hormones.[47]

This is a diagram that represents and describer what hormones are and their activity in the bloodstream. Hormones flow in and out of the bloodstream and are able to bind to Target cells to activate the role of the hormone. This is with the help of the bloodstream flow and the secreting cell. Hormones regulate: metabolism, growth and development, tissue function, sleep, reproduction, etc. This diagram also lists the important hormones in a human body.

The formation of a complex with a binding protein has several benefits: the effective half-life of the bound hormone is increased, and a reservoir of bound hormones is created, which evens the variations in concentration of unbound hormones (bound hormones will replace the unbound hormones when these are eliminated).[48] An example of the usage of hormone-binding proteins is in the thyroxine-binding protein which carries up to 80% of all thyroxine in the body, a crucial element in regulating the metabolic rate.[49]


هرمونات بشرية هامة

التهجي ليس ثابتاً للعديد من الهرمونات. Current North American and international usage is estrogen, gonadotropin, while British usage retains the Greek diphthong in oestrogen and the unvoiced aspirant h in gonadotrophin.

البنية الاسم الاختصار النسيج الخلايا الآلية النسيج
المستهدف
التأثير
amine - tryptophan Melatonin (N-acetyl-5-methoxytryptamine) الغدة الصنوبرية pinealocyte antioxidant and causes drowsiness
amine - tryptophan سيراتونين 5-HT CNS, GI tract enterochromaffin cell يتحكم في المزاج, والشهية والنوم
amine - tyrosine Thyroxine (or tetraiodothyronine) (a الهرمون الدرقي) T4 الغدة الدرقية thyroid epithelial cell مباشر less active form of الهرمون الدرقي: increase the basal metabolic rate & sensitivity to catecholamines,

affect تخليق البروتين

amine - tyrosine Triiodothyronine (هرمون درقي) T3 الغدة الدرقية thyroid epithelial cell مباشر potent form of thyroid hormone: increase the basal metabolic rate & sensitivity to catecholamines,

affect تخليق البروتين

amine - tyrosine (cat) إپينفرين (أو أدرينالين) EPI adrenal medulla chromaffin cell Fight-or-flight response:

يرفع امداد الاكسجين و الگلوكوز إلى المخ و العضلات (برفع نبض القلب وحجم الضخ, واتساع الأوعية, مما يرفع catalysis of گليكوجين في الكبد, وتكسير الدهون في الخلايا الدهنية. يوسع الحدقة Suppress non-emergency bodily processes (e.g. الهضم) Suppress جهاز المناعة

amine - tyrosine (cat) نور إپينفرين (أو نور أدرينالين) NRE adrenal medulla chromaffin cell Fight-or-flight response:

Boosts the supply of oxygen and glucose to the brain and muscles (by increasing heart rate and stroke volume, vasoconstriction and increased blood pressure, breakdown of lipids in fat cells. Increase skeletal muscle readiness.

amine - tyrosine (cat) Dopamine (or prolactin inhibiting hormone DPM, PIH or DA كلية, hypothalamus Chromaffin cells in kidney
Dopamine neurons of the arcuate nucleus in hypothalamus
Increase heart rate and blood pressure
Inhibit release of prolactin and TRH from النخامية الأمامية
پپتيد Antimullerian hormone (أو mullerian inhibiting factor or hormone) AMH الخصيتان خلايا سترولي Inhibit release of prolactin و TRH منالنخامية الأمامية
پپتيد Adiponectin Acrp30 adipose tissue
پپتيد Adrenocorticotropic hormone (or corticotropin) ACTH النخامية الأمامية corticotrope cAMP synthesis of corticosteroids (glucocorticoids and androgens) في adrenocortical cells
پپتيد Angiotensinogen and angiotensin AGT كبد IP3 vasoconstriction

release of aldosterone من adrenal cortex dipsogen.

پپتيد Antidiuretic hormone (or vasopressin, arginine vasopressin) ADH النخامية الخلفية Parvocellular neurosecretory neurons in hypothalamus
Magnocellular neurosecretory cells in posterior pituitary
varies retention of water in كليةs
moderate vasoconstriction
Release ACTH في النخامية الأمامية
پپتيد Atrial-natriuretic peptide (or atriopeptin) ANP heart cGMP
پپتيد Calcitonin CT الغدة الدرقية parafollicular cell cAMP يبني العظم ويخفض كالسيوم الدم.
پپتيد Cholecystokinin CCK الاثنى عشر Release of digestive enzymes من البنكرياس

يطلق الصفراء من gallbladder يكبت الجوع

پپتيد Corticotropin-releasing hormone CRH hypothalamus cAMP Release ACTH من النخامية الأمامية
پپتيد Erythropoietin EPO كلية Extraglomerular mesangial cells Stimulate erythrocyte production
پپتيد Follicle-stimulating hormone FSH النخامية الأمامية gonadotrope cAMP In female: stimulates maturation of Graafian follicles in مبيض.

In male: spermatogenesis, يحسـّن انتاج androgen-binding protein by the خلايا سرتولي في الخصيتان

پپتيد گاسترين GRP المعدة, الاثنى عشر الخلايا G Secretion of gastric acid by parietal cells
پپتيد Ghrelin المعدة P/D1 cell Stimulate appetite,

secretion of growth hormone from anterior pituitary gland

پپتيد جلوكاجون GCG البنكرياس خلايا ألفا cAMP glycogenolysis and gluconeogenesis في كبد

increases blood glucose level

پپتيد Gonadotropin-releasing hormone GnRH الوطاء IP3 Release of FSH and LH from النخامية الأمامية.
پپتيد الهرمون المحفز لهرمون النمو GHRH الوطاء IP3 Release GH from النخامية الأمامية
پپتيد Human chorionic gonadotropin hCG المشيمة syncytiotrophoblast cells cAMP promote maintenance of corpus luteum during beginning of pregnancy

Inhibit immune response, towards the human embryo.

پپتيد لاكتوجين المشيمة HPL المشيمة increase production of insulin and IGF-1

increase insulin resistance and carbohydrate intolerance

پپتيد Growth hormone GH or hGH النخامية الأمامية somatotropes stimulates growth and cell reproduction

Release Insulin-like growth factor 1 من الكبد

پپتيد Inhibin الخصية, المبيض, fetus خلايا سترولي بالخصيتين
granulosa cells of ovary
trophoblasts in fetus
النخامية الأمامية Inhibit production of FSH
پپتيد إنسولين INS البنكرياس خلايا بيتا tyrosine kinase Intake of glucose, glycogenesis and glycolysis in كبد و العضلات مما يستهلكه الدم من الدهون وتخليق حليسريدات الثلاثية في adipocytes

Other anabolic effects

ييتيد Insulin-like growth factor (سوماتودسين) IGF الكبد Hepatocytes tyrosine kinase insulin-like effects

regulate cell growth and development

ييتيد ليبتين LEP adipose tissue نقص الشهية وزيادة الأيض.
ييتيد Luteinizing hormone LH النخامية الأمامية gonadotropes cAMP في الإناث: ovulation

في الذكور: تحفز Leydig cell انتاج التستوستيرون

ييتيد Melanocyte stimulating hormone MSH or α-MSH النخامية الأمامية/pars intermedia Melanotroph cAMP melanogenesis by melanocytes in skin and hair
ييتيد اوكسيتوسين OXT النخامية الخلفية Magnocellular neurosecretory cells IP3 release breast milk

انقباض عنق الرحم و المهبل Involved in orgasm, trust between people.[50] and circadian homeostasis (body temperature, activity level, wakefulness) [51].

پپتيد Parathyroid hormone PTH parathyroid gland الجاردرقية chief cell cAMP increase blood Ca2+: *indirectly stimulate osteoclasts

(Slightly) decrease blood فوسفات:

پپتيد Prolactin PRL النخامية الأمامية, uterus lactotrophs of anterior pituitary
Decidual cells of uterus
milk production in mammary glands
sexual gratification after sexual acts
پپتيد Relaxin RLN uterus Decidual cells Unclear in humans
پپتيد Secretin SCT الاثنى عشر S cell Secretion of bicarbonate from كبد, pancreas and duodenal Brunner's glands

Enhances effects of cholecystokinin Stops production of gastric juice

پپتيد Somatostatin SRIF hypothalamus, islets of Langerhans, gastrointestinal system delta cells in islets
Neuroendocrince cells of the Periventricular nucleus in hypothalamus
Inhibit release of GH and TRH from النخامية الأمامية
Suppress release of gastrin, cholecystokinin (CCK), secretin, motilin, vasoactive intestinal peptide (VIP), gastric inhibitory polypeptide (GIP), enteroglucagon in gastrointestinal system
Lowers rate of gastric emptying

Reduces smooth muscle contractions and blood flow within the intestine [52]
Inhibit release of insulin from beta cells [53]
Inhibit release of glucagon from beta cells [53]
Suppress the exocrine secretory action of pancreas.

پپتيد Thrombopoietin TPO كبد, كلية, striated muscle Myocytes megakaryocytes produce platelets[54]
پپتيد Thyroid-stimulating hormone (or thyrotropin) TSH النخامية الأمامية thyrotropes cAMP الغدة الدرقية secrete thyroxine (T4) and triiodothyronine (T3)
پپتيد Thyrotropin-releasing hormone TRH hypothalamus Parvocellular neurosecretory neurons IP3 النخامية الأمامية Release thyroid-stimulating hormone (primarily)
Stimulate prolactin release
steroid - glu. Cortisol adrenal cortex (zona fasciculata and zona reticularis cells) direct Stimulation of gluconeogenesis

Inhibition of glucose uptake in muscle and adipose tissue Mobilization of amino acids from extrahepatic tissues Stimulation of fat breakdown in adipose tissue anti-inflammatory and immunosuppressive

steroid - min. Aldosterone adrenal cortex (zona glomerulosa) direct Increase blood volume by reabsorption of sodium in kidneys (primarily)

Potassium and H+ secretion in kidney.

steroid - sex (and) Testosterone الخصيتان Leydig cells direct Anabolic: growth of muscle mass and strength, increased bone density, growth and strength,

Virilizing: maturation of sex organs, formation of scrotum, deepening of voice, growth of beard and axillary hair.

steroid - sex (and) Dehydroepiandrosterone DHEA الخصيتان, مبيض, كلية Zona fasciculata and Zona reticularis cells of kidney
theca cells of ovary
Leydig cellss of testes
direct Virilization, anabolic
steroid - sex (and) Androstenedione adrenal glands, gonads direct Substrate for estrogen
steroid - sex (and) Dihydrotestosterone DHT multiple direct
steroid - sex (est) Estradiol E2 females: مبيض, males الخصيتان females: granulosa cells, males: Sertoli cell direct Females:

Structural:

بروتين synthesis:

  • increase hepatic production of binding proteins

Coagulation:

Increase HDL, triglyceride, height growth Decrease LDL, fat depositition Fluid balance:

Gastrointestinal tract:

  • reduce bowel motility
  • increase cholesterol in bile

Melanin:

Cancer: support hormone-sensitive breast cancers [55] Suppression of production in the body of estrogen is a treatment for these cancers. Lung function:

Males: Prevent apoptosis of germ cells[57]

steroid - sex (est) Estrone مبيض granulosa cells, Adipocytes direct
steroid - sex (est) Estriol placenta syncytiotrophoblast direct
steroid - sex (pro) Progesterone مبيض, adrenal glands, placenta (when pregnant) Granulosa cells theca cells of ovary direct Support pregnancy[58]:

Convert endometrium to secretory stage Make cervical mucus permeable to sperm. Inhibit immune response, e.g. towards the human embryo. Decrease uterine smooth muscle contractility[58] Inhibit lactation Inhibit onset of labor. Support fetal production of adrenal mineralo- and glucosteroids.

Other: Raise epidermal growth factor-1 levels Increase core temperature during ovulation[59] Reduce spasm and relax smooth muscle (widen bronchi and regulate mucus) Antiinflammatory Reduce gall-bladder activity[60] Normalize blood clotting and vascular tone, zinc and copper levels, cell oxygen levels, and use of fat stores for energy. Assist in thyroid function and bone growth by osteoblasts Relsilience in bone, teeth, gums, joint, tendon, ligament and skin Healing by regulating collagen Nerve function and healing by regulating myelin Prevent endometrial cancer by regulating effects of estrogen.

sterol Calcitriol (1,25-dihydroxyvitamin D3) skin/proximal tubule of kidneys direct Active form of vitamin D3

Increase absorption of calcium and phosphate from gastrointestinal tract and kidneys inhibit release of PTH

sterol Calcidiol (25-hydroxyvitamin D3) skin/proximal tubule of kidneys direct Inactive form of Vitamin D3
eicosanoid Prostaglandins PG seminal vesicle
eicosanoid Leukotrienes LT white blood cells
eicosanoid Prostacyclin PGI2 endothelium
eicosanoid Thromboxane TXA2 platelets
Prolactin releasing hormone PRH hypothalamus Release prolactin from النخامية الأمامية
Lipotropin PRH النخامية الأمامية Corticotropes lipolysis and steroidogenesis,
stimulates melanocytes to produce melanin
Brain natriuretic peptide BNP heart Cardiac myocytes (To a minor degree than ANP) reduce blood pressure by:

reducing systemic vascular resistance, reducing blood water, sodium and fats

See also

المصادر

  1. ^ Neave N (2008). Hormones and behaviour: a psychological approach. Cambridge: Cambridge Univ. Press. ISBN 978-0-521-69201-4.
  2. ^ Gibson CL (2010). "Hormones and Behaviour: A Psychological Approach (review)". Perspectives in Biology and Medicine. Project Muse. 53 (1): 152–155. doi:10.1353/pbm.0.0141. ISSN 1529-8795. S2CID 72100830.
  3. ^ "Hormones". MedlinePlus. U.S. National Library of Medicine.
  4. ^ "Hormone - The hormones of plants". Encyclopedia Britannica (in الإنجليزية). Retrieved 2021-01-05.
  5. ^ Ruhs S, Nolze A, Hübschmann R, Grossmann C (July 2017). "30 Years of the Mineralocorticoid Receptor: Nongenomic effects via the mineralocorticoid receptor". The Journal of Endocrinology. 234 (1): T107–T124. doi:10.1530/JOE-16-0659. PMID 28348113.
  6. ^ Wang ZY, Seto H, Fujioka S, Yoshida S, Chory J (March 2001). "BRI1 is a critical component of a plasma-membrane receptor for plant steroids". Nature. 410 (6826): 380–3. Bibcode:2001Natur.410..380W. doi:10.1038/35066597. PMID 11268216. S2CID 4412000.
  7. ^ Miller BF, Keane CB (1997). Miller-Keane Encyclopedia & dictionary of medicine, nursing & allied health (6th ed.). Philadelphia: Saunders. ISBN 0-7216-6278-1. OCLC 36465055.
  8. ^ "Plant Hormones/Nutrition". www2.estrellamountain.edu. Archived from the original on 2021-01-09. Retrieved 2021-01-07.
  9. ^ Wisse B (13 June 2021). "Endocrine glands". MedlinePlus. U.S. National Library of Medicine. Retrieved November 18, 2021.
  10. ^ Nussey S, Whitehead S (2001). Endocrinology: an integrated approach. Oxford: Bios Scientific Publ. ISBN 978-1-85996-252-7. PMID 20821847.
  11. ^ أ ب Belfiore A, LeRoith PE (2018). Principles of Endocrinology and Hormone Action. Cham: Springer. ISBN 978-3-319-44675-2. OCLC 1021173479.
  12. ^ Molina PE, ed. (2018). Endocrine Physiology. McGraw-Hill Education. ISBN 978-1-260-01935-3. OCLC 1034587285.
  13. ^ أ ب Whippo CW, Hangarter RP (May 2006). "Phototropism: bending towards enlightenment". The Plant Cell. 18 (5): 1110–9. doi:10.1105/tpc.105.039669. PMC 1456868. PMID 16670442.
  14. ^ Wieland OP, De Ropp RS, Avener J (April 1954). "Identity of auxin in normal urine". Nature. 173 (4408): 776–7. Bibcode:1954Natur.173..776W. doi:10.1038/173776a0. PMID 13165644. S2CID 4225835.
  15. ^ Holland JJ, Roberts D, Liscum E (2009-05-01). "Understanding phototropism: from Darwin to today". Journal of Experimental Botany. 60 (7): 1969–78. doi:10.1093/jxb/erp113. PMID 19357428.
  16. ^ "Proceedings of the Physiological Society, March 10, 1894. No. I". The Journal of Physiology. 16 (3–4): i–viii. April 1894. doi:10.1113/jphysiol.1894.sp000503. PMC 1514529. PMID 16992168.
  17. ^ Oliver G, Schäfer EA (July 1895). "The Physiological Effects of Extracts of the Suprarenal Capsules". The Journal of Physiology. 18 (3): 230–276. doi:10.1113/jphysiol.1895.sp000564. PMC 1514629. PMID 16992252.
  18. ^ Bayliss WM, Starling EH (1968). "The Mechanism of Pancreatic Secretion". In Leicester HM (ed.). Source Book in Chemistry, 1900–1950. Harvard University Press. pp. 311–313. doi:10.4159/harvard.9780674366701.c111. ISBN 978-0-674-36670-1.
  19. ^ أ ب Molina PE (2018). Endocrine physiology. McGraw-Hill Education. ISBN 978-1-260-01935-3. OCLC 1034587285.
  20. ^ Lenard J (April 1992). "Mammalian hormones in microbial cells". Trends in Biochemical Sciences. 17 (4): 147–50. doi:10.1016/0968-0004(92)90323-2. PMID 1585458.
  21. ^ Janssens PM (1987). "Did vertebrate signal transduction mechanisms originate in eukaryotic microbes?". Trends in Biochemical Sciences. 12: 456–459. doi:10.1016/0968-0004(87)90223-4.
  22. ^ Marieb E (2014). Anatomy & physiology. Glenview, IL: Pearson Education, Inc. ISBN 978-0-321-86158-0.
  23. ^ Heyland A, Hodin J, Reitzel AM (January 2005). "Hormone signaling in evolution and development: a non-model system approach". BioEssays. 27 (1): 64–75. doi:10.1002/bies.20136. PMID 15612033.
  24. ^ Wang YH, Irving HR (April 2011). "Developing a model of plant hormone interactions". Plant Signaling & Behavior. 6 (4): 494–500. Bibcode:2011PlSiB...6..494W. doi:10.4161/psb.6.4.14558. PMC 3142376. PMID 21406974.
  25. ^ "Signal relay pathways". Khan Academy. Retrieved 2019-11-13.
  26. ^ Lodish H, Berk A, Zipursky SL, Matsudaira P, Baltimore D, Darnell J (2000). "G Protein –Coupled Receptors and Their Effectors". Molecular Cell Biology (4th ed.).
  27. ^ Rosenbaum DM, Rasmussen SG, Kobilka BK (May 2009). "The structure and function of G-protein-coupled receptors". Nature. 459 (7245): 356–63. Bibcode:2009Natur.459..356R. doi:10.1038/nature08144. PMC 3967846. PMID 19458711.
  28. ^ Beato M, Chávez S, Truss M (April 1996). "Transcriptional regulation by steroid hormones". Steroids. 61 (4): 240–51. doi:10.1016/0039-128X(96)00030-X. PMID 8733009. S2CID 20654561.
  29. ^ Hammes SR (March 2003). "The further redefining of steroid-mediated signaling". Proceedings of the National Academy of Sciences of the United States of America. 100 (5): 2168–70. Bibcode:2003PNAS..100.2168H. doi:10.1073/pnas.0530224100. PMC 151311. PMID 12606724.
  30. ^ Lall S (2013). Clearopathy. India: Partridge Publishing India. p. 1. ISBN 978-1-4828-1588-7.
  31. ^ Campbell M, Jialal I (2019). "Physiology, Endocrine Hormones". StatPearls. StatPearls Publishing. PMID 30860733. Retrieved 13 November 2019.
  32. ^ Röder PV, Wu B, Liu Y, Han W (March 2016). "Pancreatic regulation of glucose homeostasis". Experimental & Molecular Medicine. 48 (3): e219. doi:10.1038/emm.2016.6. PMC 4892884. PMID 26964835.
  33. ^ أ ب Shah SB, Saxena R (2012). Allergy-hormone links. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd. ISBN 978-93-5025-013-6. OCLC 761377585.
  34. ^ "Eicosanoids". www.rpi.edu. Retrieved 2017-02-08.
  35. ^ أ ب ت ث ج ح Silverthorn DU, Johnson BR, Ober WC, Ober CW (2016). Human physiology : an integrated approach (Seventh ed.). San Francisco: Pearson. ISBN 978-0-321-98122-6. OCLC 890107246.
  36. ^ "Hormone Therapy". Cleveland Clinic.
  37. ^ Sfetcu N (2014-05-02). Health & Drugs: Disease, Prescription & Medication (in الإنجليزية). Nicolae Sfetcu.
  38. ^ Nelson, R. J. (2021). Hormones & behavior. In R. Biswas-Diener & E. Diener (Eds), Noba textbook series: Psychology. Champaign, IL: DEF publishers. Retrieved from http://noba.to/c6gvwu9m
  39. ^ (in en)Hormones and Behavior: Basic Concepts, Elsevier, 2010, pp. 97–105, doi:10.1016/b978-0-08-045337-8.00236-9, ISBN 978-0-08-045337-8, https://linkinghub.elsevier.com/retrieve/pii/B9780080453378002369, retrieved on 2021-11-18 
  40. ^ Garland T, Zhao M, Saltzman W (August 2016). "Hormones and the Evolution of Complex Traits: Insights from Artificial Selection on Behavior". Integrative and Comparative Biology. 56 (2): 207–24. doi:10.1093/icb/icw040. PMC 5964798. PMID 27252193.
  41. ^ Pfaff DW, Rubin RT, Schneider JE, Head GA (2018). Principles of hormone/behavior relations (in الإنجليزية البريطانية) (2nd ed.). London, United Kingdom: Academic Press. ISBN 978-0-12-802667-0. OCLC 1022119040.
  42. ^ Reece JB, Urry LA, Cain ML, Wasserman SA, Minorsky PV, Jackson RB, Campbell NA (2014). Campbell biology (Tenth ed.). Boston: Pearson. ISBN 978-0-321-77565-8. OCLC 849822337.
  43. ^ Siegel A, Sapru H, Hreday N, Siegel H (2006). Essential neuroscience. Philadelphia: Lippincott Williams & Wilkins. ISBN 0-7817-5077-6. OCLC 60650938.
  44. ^ أ ب Purves D, Williams SM (2001). Neuroscience (2nd ed.). Sunderland, Mass.: Sinauer Associates. ISBN 0-87893-742-0. OCLC 44627256.
  45. ^ Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). Molecular biology of the cell (4th ed.). New York: Garland Science. ISBN 0-8153-3218-1. OCLC 48122761.
  46. ^ أ ب Purves WK, Kirkwood W (2001). Life, the science of biology (6th ed.). Sunderland, MA: Sinauer Associates. ISBN 0-7167-3873-2. OCLC 45064683.
  47. ^ "Hormones". OpenStaxCollege (in الإنجليزية). 2013-03-06.
  48. ^ Boron WF, Boulpaep EL. Medical physiology: a cellular and molecular approach. Updated 2. Philadelphia, Pa: Saunders Elsevier; 2012.
  49. ^ Oppenheimer JH (1968-05-23). "Role of Plasma Proteins in the Binding, Distribution and Metabolism of the Thyroid Hormones". New England Journal of Medicine (in الإنجليزية). 278 (21): 1153–1162. doi:10.1056/NEJM196805232782107. ISSN 0028-4793. PMID 4172185.
  50. ^ Kosfeld M et al. (2005) Oxytocin increases trust in humans. Nature 435:673-676. PDF PMID 15931222
  51. ^ Scientific American Mind, "Rhythm and Blues"; June/July 2007; Scientific American Mind; by Ulrich Kraft
  52. ^ http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/otherendo/somatostatin.html Colorado State University - Biomedical Hypertextbooks - Somatostatin
  53. ^ أ ب Physiology at MCG 5/5ch4/s5ch4_17
  54. ^ Kaushansky K. Lineage-specific hematopoietic growth factors. N Engl J Med 2006;354:2034-45. PMID 16687716.
  55. ^ Hormonal Therapy
  56. ^ Massaro D, Massaro GD (2004). "Estrogen regulates pulmonary alveolar formation, loss, and regeneration in mice". American Journal of Physiology. Lung Cellular and Molecular Physiology. 287 (6): L1154-9. PMID 15298854 url=http://ajplung.physiology.org/cgi/content/full/287/6/L1154. {{cite journal}}: Missing pipe in: |id= (help)
  57. ^ Pentikäinen V, Erkkilä K, Suomalainen L, Parvinen M, Dunkel L. Estradiol Acts as a Germ Cell Survival Factor in the Human Testis in vitro. The Journal of Clinical Endocrinology & Metabolism 2006;85:2057-67 PMID 10843196
  58. ^ أ ب Placental Hormones
  59. ^ Physiology at MCG 5/5ch9/s5ch9_13
  60. ^ Hould F, Fried G, Fazekas A, Tremblay S, Mersereau W (1988). "Progesterone receptors regulate gallbladder motility". J Surg Res. 45 (6): 505–12. PMID 3184927.{{cite journal}}: CS1 maint: multiple names: authors list (link)

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