Prolactin

Last updated

PRL
PRL structure.png
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases PRL , GHA1, prolactin
External IDs OMIM: 176760; MGI: 97762; HomoloGene: 732; GeneCards: PRL; OMA:PRL - orthologs
Orthologs
SpeciesHumanMouse
Entrez

5617

19109

Ensembl

ENSG00000172179

ENSMUSG00000021342

UniProt

P01236

P06879

RefSeq (mRNA)

NM_000948
NM_001163558

NM_001163530
NM_011164

RefSeq (protein)

NP_000939
NP_001157030

NP_001157002
NP_035294

Location (UCSC) Chr 6: 22.29 – 22.3 Mb Chr 13: 27.24 – 27.25 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Prolactin (PRL), also known as lactotropin and mammotropin, is a protein best known for its role in enabling mammals to produce milk. It is influential in over 300 separate processes in various vertebrates, including humans. [5] Prolactin is secreted from the pituitary gland in response to eating, mating, estrogen treatment, ovulation and nursing. It is secreted heavily in pulses in between these events. Prolactin plays an essential role in metabolism, regulation of the immune system and pancreatic development. [6] [7]

Discovered in non-human animals around 1930 by Oscar Riddle [8] and confirmed in humans in 1970 by Henry Friesen, [9] prolactin is a peptide hormone, encoded by the PRL gene. [10]

In mammals, prolactin is associated with milk production; in fish it is thought to be related to the control of water and salt balance. Prolactin also acts in a cytokine-like manner and as an important regulator of the immune system. It has important cell cycle-related functions as a growth-, differentiating- and anti-apoptotic factor. As a growth factor, binding to cytokine-like receptors, it influences hematopoiesis and angiogenesis and is involved in the regulation of blood clotting through several pathways. The hormone acts in endocrine, autocrine, and paracrine manners through the prolactin receptor and numerous cytokine receptors. [5]

Pituitary prolactin secretion is regulated by endocrine neurons in the hypothalamus. The most important of these are the neurosecretory tuberoinfundibulum (TIDA) neurons of the arcuate nucleus that secrete dopamine (a.k.a. Prolactin Inhibitory Hormone) to act on the D2 receptors of lactotrophs, causing inhibition of prolactin secretion. Thyrotropin-releasing hormone has a stimulatory effect on prolactin release, although prolactin is the only anterior pituitary hormone whose principal control is inhibitory.

Several variants and forms are known per species. Many fish have variants prolactin A and prolactin B. Most vertebrates, including humans, also have the closely related somatolactin. In humans, 14, 16, and 22 kDa variants exist. [11]

Function

In humans

Prolactin has a wide variety of effects. It stimulates the mammary glands to produce milk (lactation): increased serum concentrations of prolactin during pregnancy cause enlargement of the mammary glands and prepare for milk production, which normally starts when levels of progesterone fall by the end of pregnancy and a suckling stimulus is present. Prolactin plays an important role in maternal behavior. [12]

It has been shown in rats and sheep that prolactin affects lipid synthesis differentially in mammary and adipose cells. Prolactin deficiency induced by bromocriptine increased lipogenesis and insulin responsiveness in adipocytes while decreasing them in the mammary gland. [13]

In general, dopamine inhibits prolactin [14] but this process has feedback mechanisms. [15]

Elevated levels of prolactin decrease the levels of sex hormones—estrogen in women and testosterone in men. [16] The effects of mildly elevated levels of prolactin are much more variable, in women, substantially increasing or decreasing estrogen levels.

Prolactin is sometimes classified as a gonadotropin [17] although in humans it has only a weak luteotropic effect while the effect of suppressing classical gonadotropic hormones is more important. [18] Prolactin within the normal reference ranges can act as a weak gonadotropin, but at the same time suppresses gonadotropin-releasing hormone secretion. The exact mechanism by which it inhibits gonadotropin-releasing hormone is poorly understood. Although expression of prolactin receptors have been demonstrated in rat hypothalamus, the same has not been observed in gonadotropin-releasing hormone neurons. [19] Physiologic levels of prolactin in males enhance luteinizing hormone-receptors in Leydig cells, resulting in testosterone secretion, which leads to spermatogenesis. [20]

Prolactin also stimulates proliferation of oligodendrocyte precursor cells. These cells differentiate into oligodendrocytes, the cells responsible for the formation of myelin coatings on axons in the central nervous system. [21]

Other actions include contributing to pulmonary surfactant synthesis of the fetal lungs at the end of the pregnancy and immune tolerance of the fetus by the maternal organism during pregnancy. Prolactin promotes neurogenesis in maternal and fetal brains. [22] [23]

In music psychology, it is conjectured that prolactin may play a role in the pleasurable perception of sad music, as the levels of the hormone increase when a person feels sad, producing a consoling psychological effect. [24]

In other vertebrates

The primary function of prolactin in fish is osmoregulation, [25] i.e., controlling the movement of water and salts between the tissues of the fish and the surrounding water. Like mammals, however, prolactin in fish also has reproductive functions, including promoting sexual maturation and inducing breeding cycles, as well as brooding and parental care. [26] In the South American discus, prolactin may also regulate the production of a skin secretion that provides food for larval fry. [27] An increase in brooding behaviour caused by prolactin has been reported in hens. [28]

Prolactin and its receptor are expressed in the skin, specifically in the hair follicles, where they regulate hair growth and moulting in an autocrine fashion. [29] [30] Elevated levels of prolactin can inhibit hair growth, [31] and knock-out mutations in the prolactin gene cause increased hair length in cattle [32] and mice. [30] Conversely, mutations in the prolactin receptor can cause reduced hair growth, resulting in the "slick" phenotype in cattle. [32] [33] Additionally, prolactin delays hair regrowth in mice. [34]

Analogous to its effects on hair growth and shedding in mammals, prolactin in birds controls the moulting of feathers, [35] as well as the age at onset of feathering in both turkeys and chickens. [36] Pigeons, flamingos and male emperor penguins feed their young a cheese-like secretion from the upper digestive tract called crop milk, whose production is regulated by prolactin. [37] [38]

In rodents, pseudopregnancy can occur when a female is mated with a sterile male. This mating can cause bi-daily surges of prolactin which would normally occur in rodent pregnancy. [39] Prolactin surges initiate the secretion of progesterone which maintains pregnancy and hence can initiate pseudopregnancy. The false maintenance of pregnancy exhibits the outward physical symptoms of pregnancy, in the absence of a foetus. [40]

Prolactin receptor activation is essential for normal mammary gland development during puberty in mice. [41] Adult virgin female prolactin receptor knockout mice have much smaller and less developed mammary glands than their wild-type counterparts. [41] Prolactin and prolactin receptor signaling are also essential for maturation of the mammary glands during pregnancy in mice. [41]

Regulation

In humans, prolactin is produced at least in the anterior pituitary, decidua, myometrium, breast, lymphocytes, leukocytes and prostate. [42] [43]

Pituitary

Pituitary prolactin is controlled by the Pit-1 transcription factor, which binds to the gene at several sites including a proximal promoter. [43] This promoter is inhibited by dopamine and stimulated by estrogens, neuropeptides, and growth factors. [44] Estrogens can also suppress dopamine.

Interaction with neuropeptides is still a matter of active research: no specific prolactin-releasing hormone has been identified. It is known that mice react to both VIP and TRH, but humans seem to only react to TRH. There are prolactin-releasing peptides that work in vitro, but whether they deserve their name has been questioned. Oxytocin does not play a large role. Mice without a posterior pituitary do not raise their prolactin levels even with suckling and oxytocin injection, but scientists have yet to identify which specific hormone produced by this region is responsible. [45]

In birds (turkeys), VIP is a powerful prolactin-releasing factor, while peptide histidine isoleucine has almost no effect. [46]

Extrapituitary

Extrapituitary prolactin is controlled by a superdistal promoter, located 5.8 kb upstream of the pituitary start site. The promoter does not react to dopamine, estrogens, or TRH. Instead, it is stimulated by cAMP. Responsiveness to cAMP is mediated by an imperfect cAMP–responsive element and two CAAT/enhancer binding proteins (C/EBP). [43] Progesterone upregulates prolactin synthesis in the endometrium but decreases it in myometrium and breast glandular tissue. [47]

Breast and other tissues may express the Pit-1 promoter in addition to the distal promoter. Oct-1 appears able to substitute for Pit-1 in activating the promoter in breast cancer cells. [45]

Extrapituitary production of prolactin is thought to be special to humans and primates and may serve mostly tissue-specific paracrine and autocrine purposes. It has been hypothesized that in vertebrates such as mice a similar tissue-specific effect is achieved by a large family of prolactin-like proteins controlled by at least 26 paralogous PRL genes not present in primates. [43]

Stimuli

Prolactin follows diurnal and ovulatory cycles. Prolactin levels peak during REM sleep and in the early morning. Many mammals experience a seasonal cycle. [38]

During pregnancy, high circulating concentrations of estrogen and progesterone increase prolactin levels by 10- to 20-fold. Estrogen and progesterone inhibit the stimulatory effects of prolactin on milk production. The abrupt drop of estrogen and progesterone levels following delivery allow prolactin—which temporarily remains high—to induce lactation. [48]

Sucking on the nipple offsets the fall in prolactin as the internal stimulus for them is removed. The sucking activates mechanoreceptors in and around the nipple. These signals are carried by nerve fibers through the spinal cord to the hypothalamus, where changes in the electrical activity of neurons that regulate the pituitary gland increase prolactin secretion. The suckling stimulus also triggers the release of oxytocin from the posterior pituitary gland, which triggers milk let-down: Prolactin controls milk production (lactogenesis) but not the milk-ejection reflex; the rise in prolactin fills the breast with milk in preparation for the next feed. The posterior pituitary produces a yet-unidentified hormone that causes prolactin production. [45]

In usual circumstances, in the absence of galactorrhea, lactation ceases within one or two weeks following the end of breastfeeding.

Levels can rise after exercise, high-protein meals, minor surgical procedures, [49] following epileptic seizures [50] or due to physical or emotional stress. [51] [52] In a study on female volunteers under hypnosis, prolactin surges resulted from the evocation, with rage, of humiliating experiences, but not from the fantasy of nursing. [52] Stress-induced PRL changes are not linked to the posterior pituitary in rodents. [45]

Hypersecretion is more common than hyposecretion. Hyperprolactinemia is the most frequent abnormality of the anterior pituitary tumors, termed prolactinomas. Prolactinomas may disrupt the hypothalamic-pituitary-gonadal axis as prolactin tends to suppress the secretion of gonadotropin-releasing hormone from the hypothalamus and in turn decreases the secretion of follicle-stimulating hormone and luteinizing hormone from the anterior pituitary, therefore disrupting the ovulatory cycle. [53] Such hormonal changes may manifest as amenorrhea and infertility in females as well as erectile dysfunction in males. [54] [7] Inappropriate lactation (galactorrhoea) is another important clinical sign of prolactinomas.

Structure and isoforms

The structure of prolactin is similar to that of growth hormone and placental lactogen. The molecule is folded due to the activity of three disulfide bonds. Significant heterogeneity of the molecule has been described, thus bioassays and immunoassays can give different results due to differing glycosylation, phosphorylation and sulfation, as well as degradation. The non-glycosylated form of prolactin is the dominant form that is secreted by the pituitary gland. [11]

The three different sizes of prolactin are:

The levels of larger ones are somewhat higher during the early postpartum period. [58]

Prolactin receptor

Prolactin receptors are present in the mammillary glands, ovaries, pituitary glands, heart, lung, thymus, spleen, liver, pancreas, kidney, adrenal gland, uterus, skeletal muscle, skin and areas of the central nervous system. [59] When prolactin binds to the receptor, it causes it to dimerize with another prolactin receptor. This results in the activation of Janus kinase 2, a tyrosine kinase that initiates the JAK-STAT pathway. Activation also results in the activation of mitogen-activated protein kinases and Src kinase. [59]

Human prolactin receptors are insensitive to mouse prolactin. [60]

Diagnostic use

Prolactin levels may be checked as part of a sex hormone workup, as elevated prolactin secretion can suppress the secretion of follicle stimulating hormone and gonadotropin-releasing hormone, leading to hypogonadism and sometimes causing erectile dysfunction. [61]

Prolactin levels may be of some use in distinguishing epileptic seizures from psychogenic non-epileptic seizures. The serum prolactin level usually rises following an epileptic seizure. [62]

Units and unit conversions

The serum concentration of prolactin can be given in mass concentration (μg/L or ng/mL), molar concentration (nmol/L or pmol/L), or international units (typically mIU/L). The current IU is calibrated against the third International Standard for Prolactin, IS 84/500. [63] [64] Reference ampoules of IS 84/500 contain "approximately" 2.5 μg of lyophilized human prolactin [65] and have been assigned an activity of 0.053 International Units by calibrating against the previous standard. [63] [64] Measurements can be converted into mass units using this ratio of grams to IUs to obtain an equivalent in relationship to the contents of IS 84/500; [66] prolactin concentrations expressed in mIU/L can be converted to μg/L of IS 84/500 equivalent by dividing by 21.2. Previous standards had other ratios in relation to their potency on the assay measurement. For example, the previous IS (83/562) had a potency of 27.0 mIU per μg. [67] [68] [69] [70]

The first International Reference Preparation (or IRP) of human Prolactin for Immunoassay was established in 1978 (75/504 1st IRP for human prolactin) at a time when purified human prolactin was in short supply. [66] [67] Previous standards relied on prolactin from animal sources. [70] Purified human prolactin was scarce, heterogeneous, unstable, and difficult to characterize. A preparation labeled 81/541 was distributed by the WHO Expert Committee on Biological Standardization without official status and given the assigned value of 50 mIU/ampoule based on an earlier collaborative study. [66] [68] It was determined that this preparation behaved anomalously in certain immunoassays and was not suitable as an IS. [66]

Three different human pituitary extracts containing prolactin were subsequently obtained as candidates for an IS. These were distributed into ampoules coded 83/562, 83/573, and 84/500. [63] [64] [66] [69] Collaborative studies involving 20 different laboratories found little difference between these three preparations. 83/562 appeared to be the most stable. This preparation was largely free of dimers and polymers of prolactin. On the basis of these investigations, 83/562 was established as the Second IS for human prolactin. [69] Once stocks of these ampoules were depleted, 84/500 was established as the Third IS for human prolactin. [63] [66]

84/500 has nearly run out and in 2016 replacement was proposed. The new 83/573 contains 67.2 mIU per ampoule when calibrated against the third IS and contains 1.002 g of human pituitary extract each (which is then lyophilized). Each ampoule contains approximately 3.2 μg of prolactin. The assigned value will be 67 mIU per ampoule. If a fifth IS is needed, it will likely be based on recombinant protein, as WHO has not received any further donations of human pituitary extracts. [71]

Reference ranges

General guidelines for diagnosing prolactin excess (hyperprolactinemia) define the upper threshold of normal prolactin at 25 μg/L for women and 20 μg/L for men. [59] Similarly, guidelines for diagnosing prolactin deficiency (hypoprolactinemia) are defined as prolactin levels below 3 μg/L in women [72] [73] and 5 μg/L in men. [74] [75] [76] However, different assays and methods for measuring prolactin are employed by different laboratories and as such the serum reference range for prolactin is often determined by the laboratory performing the measurement. [59] [77] Furthermore, prolactin levels vary according to factors as age, [78] sex, [78] menstrual cycle stage [78] and pregnancy. [78] The circumstances surrounding a given prolactin measurement (assay, patient condition, etc.) must therefore be considered before the measurement can be accurately interpreted. [59]

The following chart illustrates the variations seen in normal prolactin measurements across different populations. Prolactin values were obtained from specific control groups of varying sizes using the IMMULITE assay. [78]

Typical prolactin values
ProbandProlactin, μg/L (ng/mL)
women, follicular phase (n = 803)
12.1
women, luteal phase (n = 699)
13.9
women, mid-cycle (n = 53)
17
women, whole cycle (n = 1555)
13.0
women, pregnant, 1st trimester (n = 39)
16
women, pregnant, 2nd trimester (n = 52)
49
women, pregnant, 3rd trimester (n = 54)
113
Men, 21–30 (n = 50)
9.2
Men, 31–40 (n = 50)
7.1
Men, 41–50 (n = 50)
7.0
Men, 51–60 (n = 50)
6.2
Men, 61–70 (n = 50)
6.9

Inter-method variability

The following table illustrates variability in reference ranges of serum prolactin between some commonly used assay methods (as of 2008), using a control group of healthy health care professionals (53 males, age 20–64 years, median 28 years; 97 females, age 19–59 years, median 29 years) in Essex, England: [77]

Assay methodMean
Prolactin		Lower limit
2.5th percentile		Upper limit
97.5th percentile
mIU/Lμg/LmIU/Lμg/LmIU/Lμg/L
Females
Centaur1687.92713.3534816.4
Immulite1969.25753.5439618.7
Access1929.06773.6340819.3
Elecsys22210.5884.1549223.2
Architect22510.6984.6244721.1
AIA [a] 2579.521053.8954820.3
Males
Access1466.89582.7427713.1
Centaur1677.88632.9726212.4
Immulite1587.45703.3028113.3
Elecsys1808.49723.4033115.6
Architect1888.87854.0131014.6
AIA [a] 2117.81893.336513.52

An example of the use of the above table is, if using the Centaur assay to estimate prolactin values in μg/L for females, the mean is 168 mIU/L (7.92 μg/L) and the reference range is 71–348 mIU/L (3.35–16.4 μg/L).

Conditions

Elevated levels

Hyperprolactinaemia, or excess serum prolactin, is associated with hypoestrogenism, anovulatory infertility, oligomenorrhoea, amenorrhoea, unexpected lactation and loss of libido in women and erectile dysfunction and loss of libido in men. [80]

Causes of Elevated Prolactin Levels

Decreased levels

Hypoprolactinemia, or serum prolactin deficiency, is associated with ovarian dysfunction in women, [72] [73] and arteriogenic erectile dysfunction, premature ejaculation, [74] oligozoospermia, asthenospermia, hypofunction of seminal vesicles and hypoandrogenism [75] in men. In one study, normal sperm characteristics were restored when prolactin levels were raised to normal values in hypoprolactinemic men. [76]

Hypoprolactinemia can result from hypopituitarism, excessive dopaminergic action in the tuberoinfundibular pathway and ingestion of D2 receptor agonists such as bromocriptine.[ citation needed ]

In medicine

Prolactin is available commercially for use in other animals, but not in humans. [81] It is used to stimulate lactation in animals. [81] The biological half-life of prolactin in humans is around 15–20 minutes. [82] The D2 receptor is involved in the regulation of prolactin secretion, and agonists of the receptor such as bromocriptine and cabergoline decrease prolactin levels while antagonists of the receptor such as domperidone, metoclopramide, haloperidol, risperidone, and sulpiride increase prolactin levels. [83] D2 receptor antagonists like domperidone, metoclopramide, and sulpiride are used as galactogogues to increase prolactin secretion in the pituitary gland and induce lactation in humans. [84]

See also

Related Research Articles

<span class="mw-page-title-main">Luteinizing hormone</span> Gonadotropin secreted by the adenohypophysis

Luteinizing hormone is a hormone produced by gonadotropic cells in the anterior pituitary gland. The production of LH is regulated by gonadotropin-releasing hormone (GnRH) from the hypothalamus. In females, an acute rise of LH known as an LH surge, triggers ovulation and development of the corpus luteum. In males, where LH had also been called interstitial cell–stimulating hormone (ICSH), it stimulates Leydig cell production of testosterone. It acts synergistically with follicle-stimulating hormone (FSH).

<span class="mw-page-title-main">Hyperprolactinaemia</span> Excess of prolactin hormone in the blood

Hyperprolactinaemia is a condition characterized by abnormally high levels of prolactin in the blood. In women, normal prolactin levels average to about 13 ng/mL, while in men, they average 5 ng/mL. The upper normal limit of serum prolactin is typically between 15 to 25 ng/mL for both genders. Levels exceeding this range indicate hyperprolactinemia.

<span class="mw-page-title-main">Follicle-stimulating hormone</span> Gonadotropin that regulates the development of reproductive processes

Follicle-stimulating hormone (FSH) is a gonadotropin, a glycoprotein polypeptide hormone. FSH is synthesized and secreted by the gonadotropic cells of the anterior pituitary gland and regulates the development, growth, pubertal maturation, and reproductive processes of the body. FSH and luteinizing hormone (LH) work together in the reproductive system.

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.

<span class="mw-page-title-main">Anterior pituitary</span> Anterior lobe of the pituitary gland

The anterior pituitary is a major organ of the endocrine system. The anterior pituitary is the glandular, anterior lobe that together with the makes up the pituitary gland (hypophysis) which, in humans, is located at the base of the brain, protruding off the bottom of the hypothalamus.

A prolactin cell is a cell in the anterior pituitary which produces prolactin in response to hormonal signals including dopamine, thyrotropin-releasing hormone and estrogen, which are stimulatory. Prolactin is responsible for actions needed for body homeostasis, the development of breasts, and for lactation. The inhibitory effects of dopamine override the stimulatory effects of TRH in non-pregnant, non-lactating sexually mature females. Depending on the sex of the individual, prolactin cells account for 20% - 50% of all cells in the anterior pituitary gland. The inhibitory effects of dopamine override the stimulatory effects of TRH in non-pregnant, non-lactating sexually mature females. Other regulators include oxytocin and progesterone.

Anovulation is when the ovaries do not release an oocyte during a menstrual cycle. Therefore, ovulation does not take place. However, a woman who does not ovulate at each menstrual cycle is not necessarily going through menopause. Chronic anovulation is a common cause of infertility.

<span class="mw-page-title-main">Pituitary adenoma</span> Tumor of the pituitary gland

Pituitary adenomas are tumors that occur in the pituitary gland. Most pituitary tumors are benign, approximately 35% are invasive and just 0.1% to 0.2% are carcinomas. Pituitary adenomas represent from 10% to 25% of all intracranial neoplasms, with an estimated prevalence rate in the general population of approximately 17%.

<span class="mw-page-title-main">Prolactinoma</span> Pituitary gland tumor which secretes the hormone prolactin

A prolactinoma is a tumor (adenoma) of the pituitary gland that produces the hormone prolactin. It is the most common type of functioning pituitary tumor. Symptoms of prolactinoma are due to abnormally high levels of prolactin in the blood (hyperprolactinemia), or due to pressure of the tumor on surrounding brain tissue and/or the optic nerves. Based on its size, a prolactinoma may be classified as a microprolactinoma or a macroprolactinoma.

Witch's milk or neonatal milk is milk secreted from the breasts of some newborn human infants of either sex. Production of neonatal milk by infants usually resolves itself and does not require treatment unless it is caused by an underlying condition or medications. It is thought to be caused by the exposure to an elevated level of estrogen to infants during pregnancy or decreased exposure of estrogen to infants after birth. Its production also may be caused by certain medications. The composition of neonatal milk is similar to maternal milk for most of their components except for fats and one type of antibody.

The prolactin receptor (PRLR) is a type I cytokine receptor encoded in humans by the PRLR gene on chromosome 5p13-14. It is the receptor for prolactin (PRL). The PRLR can also bind to and be activated by growth hormone (GH) and human placental lactogen (hPL). The PRLR is expressed in the mammary glands, pituitary gland, and other tissues. It plays an important role in lobuloalveolar development of the mammary glands during pregnancy and in lactation.

<span class="mw-page-title-main">Human placental lactogen</span> Polypeptide placental hormone in humans

Human placental lactogen (hPL), also called human chorionic somatomammotropin (hCS) or human chorionic somatotropin, is a polypeptide placental hormone, the human form of placental lactogen. Its structure and function are similar to those of human growth hormone. It modifies the metabolic state of the mother during pregnancy to facilitate energy supply to the fetus. hPL has anti-insulin properties. hPL is a hormone secreted by the syncytiotrophoblast during pregnancy. Like human growth hormone, hPL is encoded by genes on chromosome 17q22-24. It was identified in 1963.

<span class="mw-page-title-main">Hyperpituitarism</span> Medical condition

Hyperpituitarism is a condition due to the primary hypersecretion of pituitary hormones; it typically results from a pituitary adenoma. In children with hyperpituitarism, disruption of growth regulation is rare, either because of hormone hypersecretion or because of manifestations caused by local compression of the adenoma.

<span class="mw-page-title-main">Estrogen insensitivity syndrome</span> Medical condition

Estrogen insensitivity syndrome (EIS), or estrogen resistance, is a form of congenital estrogen deficiency or hypoestrogenism which is caused by a defective estrogen receptor (ER) – specifically, the estrogen receptor alpha (ERα) – that results in an inability of estrogen to mediate its biological effects in the body. Congenital estrogen deficiency can alternatively be caused by a defect in aromatase, the enzyme responsible for the biosynthesis of estrogens, a condition which is referred to as aromatase deficiency and is similar in symptomatology to EIS.

Breast development, also known as mammogenesis, is a complex biological process in primates that takes place throughout a female's life.

Hormonal regulation occurs at every stage of development. A milieu of hormones simultaneously affects development of the fetus during embryogenesis and the mother, including human chorionic gonadotropin (hCG) and progesterone (P4).

Hypogonadotropic hypogonadism (HH), is due to problems with either the hypothalamus or pituitary gland affecting the hypothalamic-pituitary-gonadal axis. Hypothalamic disorders result from a deficiency in the release of gonadotropic releasing hormone (GnRH), while pituitary gland disorders are due to a deficiency in the release of gonadotropins from the anterior pituitary. GnRH is the central regulator in reproductive function and sexual development via the HPG axis. GnRH is released by GnRH neurons, which are hypothalamic neuroendocrine cells, into the hypophyseal portal system acting on gonadotrophs in the anterior pituitary. The release of gonadotropins, LH and FSH, act on the gonads for the development and maintenance of proper adult reproductive physiology. LH acts on Leydig cells in the male testes and theca cells in the female. FSH acts on Sertoli cells in the male and follicular cells in the female. Combined this causes the secretion of gonadal sex steroids and the initiation of folliculogenesis and spermatogenesis. The production of sex steroids forms a negative feedback loop acting on both the anterior pituitary and hypothalamus causing a pulsatile secretion of GnRH. GnRH neurons lack sex steroid receptors and mediators such as kisspeptin stimulate GnRH neurons for pulsatile secretion of GnRH.

<span class="mw-page-title-main">Hypoprolactinemia</span> Medical condition

Hypoprolactinemia is a medical condition characterized by a deficiency in the serum levels of the hypothalamic-pituitary hormone prolactin.

Gonadotropin surge-attenuating factor (GnSAF) is a nonsteroidal ovarian hormone produced by the granulosa cells of small antral ovarian follicles in females. GnSAF is involved in regulating the secretion of luteinizing hormone (LH) from the anterior pituitary and the ovarian cycle. During the early to mid-follicular phase of the ovarian cycle, GnSAF acts on the anterior pituitary to attenuate LH release, limiting the secretion of LH to only basal levels. At the transition between follicular and luteal phase, GnSAF bioactivity declines sufficiently to permit LH secretion above basal levels, resulting in the mid-cycle LH surge that initiates ovulation. In normally ovulating women, the LH surge only occurs when the oocyte is mature and ready for extrusion. GnSAF bioactivity is responsible for the synchronised, biphasic nature of LH secretion.

Hormones during pregnancy are the result of an intricate interaction between hormones generated by different glands and organs. The primary hormones involved comprise human chorionic gonadotropin (hCG), progesterone, estrogen, human placental lactogen (hPL), and oxytocin. Hormones are synthesized in certain organs, including the ovaries, placenta, and pituitary gland. These hormones have essential functions in pregnancy test, maintaining the uterine lining, fetal development, preventing premature labor, and the initiation and support of labor.

References

  1. 1 2 Beltran 2008 Table 2 Archived 9 November 2011 at the Wayback Machine reports measurements in mIU/L. AIA machines are calibrated to read the correct amount of μg/L against the second international standard IS 83/562, which has a potency of 27.0 mIU per μg. [79] By converting these measurements to mIU/L, Beltran makes measurements from machines calibrated against the second and third IS comparable, because the third IS is calibrated against the second to maintain the magnitude of the IU. However, the raw readout of the machine will still be in μg/L of IS-83/562-equivalent, unlike the other machines which report in μg/L of IS-84/500-equivalent.
  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000172179 – Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000021342 – Ensembl, May 2017
  3. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. 1 2 Bole-Feysot C, Goffin V, Edery M, Binart N, Kelly PA (June 1998). "Prolactin (PRL) and its receptor: actions, signal transduction pathways and phenotypes observed in PRL receptor knockout mice". Endocrine Reviews. 19 (3): 225–68. doi: 10.1210/edrv.19.3.0334 . PMID   9626554.
  6. ↑ Ben-Jonathan N, Hugo ER, Brandebourg TD, LaPensee CR (April 2006). "Focus on prolactin as a metabolic hormone". Trends in Endocrinology and Metabolism. 17 (3): 110–116. doi:10.1016/j.tem.2006.02.005. PMID   16517173. S2CID   37979194.
  7. 1 2 Ali M, Mirza L (1 May 2021). "Morbid Obesity Due to Prolactinoma and Significant Weight Loss After Dopamine Agonist Treatment". AACE Clinical Case Reports. 7 (3): 204–206. doi:10.1016/j.aace.2021.01.004. PMC   8165126 . PMID   34095489.
  8. ↑ Bates R, Riddle O (November 1935). "The preparation of prolactin". Journal of Pharmacology and Experimental Therapeutics. 55 (3): 365–371.
  9. ↑ Friesen H, Guyda H, Hardy J (December 1970). "The biosynthesis of human growth hormone and prolactin". The Journal of Clinical Endocrinology and Metabolism. 31 (6): 611–24. doi:10.1210/jcem-31-6-611. PMID   5483096.[ permanent dead link ]
  10. ↑ Evans AM, Petersen JW, Sekhon GS, DeMars R (May 1989). "Mapping of prolactin and tumor necrosis factor-beta genes on human chromosome 6p using lymphoblastoid cell deletion mutants". Somatic Cell and Molecular Genetics. 15 (3): 203–13. doi:10.1007/BF01534871. PMID   2567059. S2CID   36302971.
  11. 1 2 3 Mizutani K, Takai Y (1 January 2018), "Prolactin", Reference Module in Biomedical Sciences, Elsevier, doi:10.1016/b978-0-12-801238-3.98018-8, ISBN   978-0-12-801238-3 , retrieved 10 January 2024
  12. ↑ Lucas BK, Ormandy CJ, Binart N, Bridges RS, Kelly PA (October 1998). "Null mutation of the prolactin receptor gene produces a defect in maternal behavior". Endocrinology. 139 (10): 4102–7. doi: 10.1210/endo.139.10.6243 . PMID   9751488.
  13. ↑ Ros M, Lobato MF, García-Ruíz JP, Moreno FJ (March 1990). "Integration of lipid metabolism in the mammary gland and adipose tissue by prolactin during lactation". Molecular and Cellular Biochemistry. 93 (2): 185–94. doi:10.1007/BF00226191. PMID   2345543. S2CID   19824793.
  14. ↑ Ben-Jonathan N (1985). "Dopamine: a prolactin-inhibiting hormone". Endocrine Reviews. 6 (4): 564–89. doi:10.1210/edrv-6-4-564. PMID   2866952.
  15. ↑ Freeman ME, Kanyicska B, Lerant A, Nagy G (October 2000). "Prolactin: structure, function, and regulation of secretion". Physiological Reviews. 80 (4): 1523–631. doi:10.1152/physrev.2000.80.4.1523. PMID   11015620.
  16. ↑ Prolactinoma—Mayo Clinic
  17. ↑ Hoehn K, Marieb EN (2007). Human Anatomy & Physiology . San Francisco: Pearson Benjamin Cummings. p. 605. ISBN   978-0-8053-5909-1.
  18. ↑ Gonadotropins at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
  19. ↑ Grattan DR, Jasoni CL, Liu X, Anderson GM, Herbison AE (September 2007). "Prolactin regulation of gonadotropin-releasing hormone neurons to suppress luteinizing hormone secretion in mice". Endocrinology. 148 (9): 4344–51. doi: 10.1210/en.2007-0403 . PMID   17569755.
  20. ↑ Hair WM, Gubbay O, Jabbour HN, Lincoln GA (July 2002). "Prolactin receptor expression in human testis and accessory tissues: localization and function". Molecular Human Reproduction. 8 (7): 606–11. doi: 10.1093/molehr/8.7.606 . PMID   12087074.
  21. ↑ Gregg C, Shikar V, Larsen P, Mak G, Chojnacki A, Yong VW, Weiss S (February 2007). "White matter plasticity and enhanced remyelination in the maternal CNS". The Journal of Neuroscience. 27 (8): 1812–23. doi:10.1523/JNEUROSCI.4441-06.2007. PMC   6673564 . PMID   17314279.
  22. ↑ Shingo T, Gregg C, Enwere E, Fujikawa H, Hassam R, Geary C, Cross JC, Weiss S (January 2003). "Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin". Science. 299 (5603): 117–20. Bibcode:2003Sci...299..117S. doi:10.1126/science.1076647. PMID   12511652. S2CID   38577726.
  23. ↑ Larsen CM, Grattan DR (February 2012). "Prolactin, neurogenesis, and maternal behaviors". Brain, Behavior, and Immunity. 26 (2): 201–9. doi:10.1016/j.bbi.2011.07.233. PMID   21820505. S2CID   27182670.
  24. ↑ Huron D (13 July 2011). "Why is sad music pleasurable? A possible role for prolactin". Musicae Scientiae. 15 (2): 146–158. doi:10.1177/1029864911401171. S2CID   45981792.
  25. ↑ Sakamoto T, McCormick SD (May 2006). "Prolactin and growth hormone in fish osmoregulation". General and Comparative Endocrinology. 147 (1): 24–30. doi:10.1016/j.ygcen.2005.10.008. PMID   16406056.
  26. ↑ Whittington CM, Wilson AB (September 2013). "The role of prolactin in fish reproduction" (PDF). General and Comparative Endocrinology. 191: 123–36. doi:10.1016/j.ygcen.2013.05.027. PMID   23791758.
  27. ↑ Khong HK, Kuah MK, Jaya-Ram A, Shu-Chien AC (May 2009). "Prolactin receptor mRNA is upregulated in discus fish (Symphysodon aequifasciata) skin during parental phase". Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology. 153 (1): 18–28. doi:10.1016/j.cbpb.2009.01.005. PMID   19272315.
  28. ↑ Jiang RS, Xu GY, Zhang XQ, Yang N (June 2005). "Association of polymorphisms for prolactin and prolactin receptor genes with broody traits in chickens". Poultry Science. 84 (6): 839–845. doi: 10.1093/ps/84.6.839 . PMID   15971519.
  29. ↑ Foitzik K, Krause K, Nixon AJ, Ford CA, Ohnemus U, Pearson AJ, Paus R (May 2003). "Prolactin and Its Receptor Are Expressed in Murine Hair Follicle Epithelium, Show Hair Cycle-Dependent Expression, and Induce Catagen". The American Journal of Pathology. 162 (5): 1611–21. doi:10.1016/S0002-9440(10)64295-2. PMC   1851183 . PMID   12707045.
  30. 1 2 Craven AJ, Ormandy CJ, Robertson FG, Wilkins RJ, Kelly PA, Nixon AJ, Pearson AJ (June 2001). "Prolactin Signaling Influences the Timing Mechanism of the Hair Follicle: Analysis of Hair Growth Cycles in Prolactin Receptor Knockout Mice". Endocrinology. 142 (6): 2533–9. doi: 10.1210/endo.142.6.8179 . PMID   11356702.
  31. ↑ Foitzik K, Krause K, Conrad F, Nakamura M, Funk W, Paus R (March 2006). "Human scalp hair follicles are both a target and a source of prolactin, which serves as an autocrine and/or paracrine promoter of apoptosis-driven hair follicle regression". The American Journal of Pathology. 168 (3): 748–56. doi:10.2353/ajpath.2006.050468. PMC   1606541 . PMID   16507890.
  32. 1 2 Littlejohn MD, Henty KM, Tiplady K, Johnson T, Harland C, Lopdell T, Sherlock RG, Li W, Lukefahr SD, Shanks BC, Garrick DJ, Snell RG, Spelman RJ, Davis SR (December 2014). "Functionally reciprocal mutations of the prolactin signalling pathway define hairy and slick cattle". Nature Communications. 5: 5861. Bibcode:2014NatCo...5.5861L. doi:10.1038/ncomms6861. PMC   4284646 . PMID   25519203.
  33. ↑ Porto-Neto LR, Bickhart DM, Landaeta-Hernandez AJ, Utsunomiya YT, Pagan M, Jimenez E, Hansen PJ, Dikmen S, Schroeder SG, Kim ES, Sun J, Crespo E, Amati N, Cole JB, Null DJ, Garcia JF, Reverter A, Barendse W, Sonstegard TS (February 2018). "Convergent Evolution of Slick Coat in Cattle through Truncation Mutations in the Prolactin Receptor". Frontiers in Genetics. 9: 57. doi: 10.3389/fgene.2018.00057 . PMC   5829098 . PMID   29527221.
  34. ↑ Craven AJ, Nixon AJ, Ashby MG, Ormandy CJ, Blazek K, Wilkins RJ, Pearson AJ (November 2006). "Prolactin delays hair regrowth in mice". The Journal of Endocrinology. 191 (2): 415–25. doi: 10.1677/joe.1.06685 . hdl: 10289/1353 . PMID   17088411.
  35. ↑ Dawson A (July 2006). "Control of molt in birds: association with prolactin and gonadal regression in starlings". General and Comparative Endocrinology. 147 (3): 314–22. doi:10.1016/j.ygcen.2006.02.001. PMID   16530194.
  36. ↑ Derks MF, Herrero-Medrano JM, Crooijmans RP, Vereijken A, Long JA, Megens HJ, Groenen MA (February 2018). "Early and late feathering in turkey and chicken: same gene but different mutations". Genetics Selection Evolution. 50 (1): 7. doi: 10.1186/s12711-018-0380-3 . PMC   5863816 . PMID   29566646.
  37. ↑ Wang Y, Wang X, Luo Y, Zhang J, Lin Y, Wu J, Zeng B, Liu L, Yan P, Liang J, Guo H, Jin L, Tang Q, Long K, Li M (8 June 2023). "Spatio-temporal transcriptome dynamics coordinate rapid transition of core crop functions in 'lactating' pigeon". PLOS Genetics. 19 (6): e1010746. doi: 10.1371/journal.pgen.1010746 . ISSN   1553-7404. PMC   10249823 . PMID   37289658.
  38. 1 2 Stewart C, Marshall CJ (2022). "Seasonality of prolactin in birds and mammals". Journal of Experimental Zoology Part A: Ecological and Integrative Physiology. 337 (9–10): 919–938. Bibcode:2022JEZA..337..919S. doi:10.1002/jez.2634. ISSN   2471-5638. PMC   9796654 . PMID   35686456.
  39. ↑ Ladyman SR, Hackwell EC, Brown RS (May 2020). "The role of prolactin in co-ordinating fertility and metabolic adaptations during reproduction". Neuropharmacology. 167: 107911. doi:10.1016/j.neuropharm.2019.107911. PMID   32058177. S2CID   208985116.
  40. ↑ Demirel MA, Suntar I, Ceribaşı S, Zengin G, Ceribaşı AO (1 August 2018). "Evaluation of the therapeutic effects of Artemisia absinthium L. on pseudopregnancy model in rats". Phytochemistry Reviews. 17 (4): 937–946. Bibcode:2018PChRv..17..937D. doi:10.1007/s11101-018-9571-3. ISSN   1572-980X. S2CID   4953983.
  41. 1 2 3 Ormandy CJ, Binart N, Kelly PA (October 1997). "Mammary gland development in prolactin receptor knockout mice". J Mammary Gland Biol Neoplasia. 2 (4): 355–64. doi:10.1023/a:1026395229025. PMID   10935023. S2CID   24217896.
  42. ↑ Ben-Jonathan N, Mershon JL, Allen DL, Steinmetz RW (December 1996). "Extrapituitary prolactin: distribution, regulation, functions, and clinical aspects". Endocrine Reviews. 17 (6): 639–69. doi: 10.1210/edrv-17-6-639 . PMID   8969972.
  43. 1 2 3 4 Gerlo S, Davis JR, Mager DL, Kooijman R (October 2006). "Prolactin in man: a tale of two promoters". BioEssays. 28 (10): 1051–5. doi:10.1002/bies.20468. PMC   1891148 . PMID   16998840.
  44. ↑ Ben-Jonathan N. (2001) Hypothalamic control of prolactin synthesis and secretion . In: Horseman ND, ed. Prolactin. Boston: Kluwer; 1 –24
  45. 1 2 3 4 Ben-Jonathan N, LaPensee CR, LaPensee EW (February 2008). [18057139 "What can we learn from rodents about prolactin in humans?"]. Endocrine Reviews. 29 (1): 1–41. doi:10.1210/er.2007-0017. PMC   2244934 . PMID   18057139.{{cite journal}}: Check |url= value (help)
  46. ↑ Kulick RS, Chaiseha Y, Kang SW, Rozenboim I, El Halawani ME (July 2005). "The relative importance of vasoactive intestinal peptide and peptide histidine isoleucine as physiological regulators of prolactin in the domestic turkey". General and Comparative Endocrinology. 142 (3): 267–73. doi:10.1016/j.ygcen.2004.12.024. PMID   15935152.
  47. ↑ Zinger M, McFarland M, Ben-Jonathan N (February 2003). "Prolactin expression and secretion by human breast glandular and adipose tissue explants". The Journal of Clinical Endocrinology and Metabolism. 88 (2): 689–96. doi: 10.1210/jc.2002-021255 . PMID   12574200.
  48. ↑ Calik-Ksepka A, Stradczuk M, Czarnecka K, Grymowicz M, Smolarczyk R (31 January 2022). "Lactational Amenorrhea: Neuroendocrine Pathways Controlling Fertility and Bone Turnover". International Journal of Molecular Sciences. 23 (3): 1633. doi: 10.3390/ijms23031633 . ISSN   1422-0067. PMC   8835773 . PMID   35163554.
  49. ↑ Melmed S, Jameson JL (2005). "333 Disorders of the Anterior Pituitary and Hypothalamus". In Jameson JN, Kasper DL, Harrison TR, Braunwald E, Fauci AS, Hauser SL, Longo DL (eds.). Harrison's principles of internal medicine (16th ed.). New York: McGraw-Hill Medical Publishing Division. ISBN   978-0-07-140235-4.
  50. ↑ Mellers JD (August 2005). "The approach to patients with "non-epileptic seizures"". Postgraduate Medical Journal. 81 (958): 498–504. doi:10.1136/pgmj.2004.029785. PMC   1743326 . PMID   16085740.
  51. ↑ "Prolactin". MedLine plus. Retrieved 24 October 2014.
  52. 1 2 Sobrinho LG (2003). "Prolactin, psychological stress and environment in humans: adaptation and maladaptation". Pituitary. 6 (1): 35–9. doi:10.1023/A:1026229810876. PMID   14674722. S2CID   1335211.
  53. ↑ Welt CK, Barbieri RL, Geffner ME (2020). "Etiology, diagnosis, and treatment of secondary amenorrhea". UpToDate. Waltham, MA. Retrieved 7 November 2013.
  54. ↑ Saleem M, Martin H, Coates P (February 2018). "Prolactin Biology and Laboratory Measurement: An Update on Physiology and Current Analytical Issues". The Clinical Biochemist. Reviews. 39 (1): 3–16. PMC   6069739 . PMID   30072818.
  55. 1 2 3 4 Sabharwal P, Glaser R, Lafuse W, Varma S, Liu Q, Arkins S, Kooijman R, Kutz L, Kelley KW, Malarkey WB (August 1992). "Prolactin synthesized and secreted by human peripheral blood mononuclear cells: an autocrine growth factor for lymphoproliferation". Proceedings of the National Academy of Sciences of the United States of America. 89 (16): 7713–6. Bibcode:1992PNAS...89.7713S. doi: 10.1073/pnas.89.16.7713 . PMC   49781 . PMID   1502189., in turn citing: Kiefer KA, Malarkey WB (January 1978). "Size heterogeneity of human prolactin in CSF and serum: experimental conditions that alter gel filtration patterns". The Journal of Clinical Endocrinology and Metabolism. 46 (1): 119–24. doi:10.1210/jcem-46-1-119. PMID   752015.
  56. ↑ Garnier PE, Aubert ML, Kaplan SL, Grumbach MM (December 1978). "Heterogeneity of pituitary and plasma prolactin in man: decreased affinity of "Big" prolactin in a radioreceptor assay and evidence for its secretion". The Journal of Clinical Endocrinology and Metabolism. 47 (6): 1273–81. doi:10.1210/jcem-47-6-1273. PMID   263349.
  57. ↑ Leite V, Cosby H, Sobrinho LG, Fresnoza MA, Santos MA, Friesen HG (October 1992). "Characterization of big, big prolactin in patients with hyperprolactinaemia". Clinical Endocrinology. 37 (4): 365–72. doi:10.1111/j.1365-2265.1992.tb02340.x. PMID   1483294. S2CID   42796831.
  58. ↑ Kamel MA, Neulen J, Sayed GH, Salem HT, Breckwoldt M (September 1993). "Heterogeneity of human prolactin levels in serum during the early postpartum period". Gynecological Endocrinology. 7 (3): 173–7. doi:10.3109/09513599309152499. PMID   8291454.
  59. 1 2 3 4 5 Mancini T, Casanueva FF, Giustina A (March 2008). "Hyperprolactinemia and prolactinomas". Endocrinology and Metabolism Clinics of North America. 37 (1): 67–99, viii. doi:10.1016/j.ecl.2007.10.013. PMID   18226731.
  60. ↑ Utama FE, LeBaron MJ, Neilson LM, Sultan AS, Parlow AF, Wagner KU, Rui H (March 2006). "Human prolactin receptors are insensitive to mouse prolactin: implications for xenotransplant modeling of human breast cancer in mice". The Journal of Endocrinology. 188 (3): 589–601. doi: 10.1677/joe.1.06560 . PMID   16522738.
  61. ↑ Al-Chalabi M, Bass AN, Alsalman I (2023), "Physiology, Prolactin", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29939606 , retrieved 10 January 2024
  62. ↑ Banerjee S, Paul P, Talib VJ (August 2004). "Serum prolactin in seizure disorders". Indian Pediatrics. 41 (8): 827–31. PMID   15347871.
  63. 1 2 3 4 Schulster D, Gaines Das RE, Jeffcoate SL (April 1989). "International Standards for human prolactin: calibration by international collaborative study". The Journal of Endocrinology. 121 (1): 157–66. doi:10.1677/joe.0.1210157. PMID   2715755.
  64. 1 2 3 "WHO Expert Committee on Biological Standardization" (PDF). Thirty-ninth Report, WHO Technical Report Series. World Health Organization. 1989. Retrieved 3 June 2009. 86.1520, WHO/BS documents: 86.1520 Add 1, 88.1596
  65. ↑ "WHO International Standard, Prolactin, Human. NIBSC code: 84/500, Instructions for use" (PDF). NIBSC / Health Protection Agency. 1989. Archived from the original (PDF) on 3 October 2011. Retrieved 21 March 2011.
  66. 1 2 3 4 5 6 Canadian Society of Clinical Chemists (December 1992). "Canadian Society of Clinical Chemists position paper: standardization of selected polypeptide hormone measurements". Clinical Biochemistry. 25 (6): 415–24. doi:10.1016/0009-9120(92)90030-V. PMID   1477965.
  67. 1 2 Gaines Das RE, Cotes PM (January 1979). "International Reference Preparation of human prolactin for immunoassay: definition of the International Unit, report of a collaborative study and comparison of estimates of human prolactin made in various laboratories". The Journal of Endocrinology. 80 (1): 157–68. doi:10.1677/joe.0.0800157. PMID   429949.
  68. 1 2 "WHO Expert Committee on Biological Standardization" (PDF). Thirty-fifth Report, WHO Technical Report Series. World Health Organization. 1985. Retrieved 21 March 2011.
  69. 1 2 3 "WHO Expert Committee on Biological Standardization" (PDF). Thirty-seventh Report, WHO Technical Report Series. World Health Organization. 1987. Retrieved 21 March 2011.[ dead link ]
  70. 1 2 Bangham DR, Mussett MV, Stack-Dunne MP (1963). "The Second International Standard for Prolactin". Bulletin of the World Health Organization. 29 (6): 721–8. PMC   2555104 . PMID   14107744.
  71. ↑ Ferguson J (2016). "WHO International Collaborative Study of the Proposed 4th International Standard for Prolactin, Human".
  72. 1 2 Kauppila A, Martikainen H, Puistola U, Reinilä M, Rönnberg L (March 1988). "Hypoprolactinemia and ovarian function". Fertility and Sterility. 49 (3): 437–41. doi:10.1016/s0015-0282(16)59769-6. PMID   3342895.
  73. 1 2 Schwärzler P, Untergasser G, Hermann M, Dirnhofer S, Abendstein B, Berger P (October 1997). "Prolactin gene expression and prolactin protein in premenopausal and postmenopausal human ovaries". Fertility and Sterility. 68 (4): 696–701. doi: 10.1016/S0015-0282(97)00320-8 . PMID   9341613.
  74. 1 2 Corona G, Mannucci E, Jannini EA, Lotti F, Ricca V, Monami M, Boddi V, Bandini E, Balercia G, Forti G, Maggi M (May 2009). "Hypoprolactinemia: a new clinical syndrome in patients with sexual dysfunction". The Journal of Sexual Medicine. 6 (5): 1457–66. doi:10.1111/j.1743-6109.2008.01206.x. PMID   19210705.
  75. 1 2 Gonzales GF, Velasquez G, Garcia-Hjarles M (1989). "Hypoprolactinemia as related to seminal quality and serum testosterone". Archives of Andrology. 23 (3): 259–65. doi:10.3109/01485018908986849. PMID   2619414.
  76. 1 2 Ufearo CS, Orisakwe OE (September 1995). "Restoration of normal sperm characteristics in hypoprolactinemic infertile men treated with metoclopramide and exogenous human prolactin". Clinical Pharmacology and Therapeutics. 58 (3): 354–9. doi:10.1016/0009-9236(95)90253-8. PMID   7554710. S2CID   1735908.
  77. 1 2 Table 2 Archived 9 November 2011 at the Wayback Machine in Beltran L, Fahie-Wilson MN, McKenna TJ, Kavanagh L, Smith TP (October 2008). "Serum total prolactin and monomeric prolactin reference intervals determined by precipitation with polyethylene glycol: evaluation and validation on common immunoassay platforms". Clinical Chemistry. 54 (10): 1673–81. doi: 10.1373/clinchem.2008.105312 . PMID   18719199.
  78. 1 2 3 4 5 Prolaktin Archived 28 July 2011 at the Wayback Machine at medical.siemens.com—reference ranges as determined from the IMMULITE assay method
  79. ↑ "CL AIA-PACK® Prolactin TEST CUP" (PDF).
  80. ↑ Melmed S, Kleinberg D 2008 Anterior pituitary. 1n: Kronenberg HM, Melmed S, Polonsky KS, Larsen PR, eds. Willams textbook of endocrinology. 11th ed. Philadelphia: Saunders Elsevier; 185–261
  81. 1 2 Coutts RT, Smail GA (12 May 2014). Polysaccharides Peptides and Proteins: Pharmaceutical Monographs. Elsevier. pp. 153–. ISBN   978-1-4831-9612-1.
  82. ↑ D.F. Horrobin (6 December 2012). Prolactin: Physiology and Clinical Significance. Springer Science & Business Media. pp. 13–. ISBN   978-94-010-9695-9.
  83. ↑ Martin H. Johnson (14 December 2012). Essential Reproduction. John Wiley & Sons. pp. 40–. ISBN   978-1-118-42388-2.
  84. ↑ Jan Riordan (January 2005). Breastfeeding and Human Lactation. Jones & Bartlett Learning. pp. 468–. ISBN   978-0-7637-4585-1.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.