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Prolactin

Drugs and Chemicals · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

A lactogenic hormone secreted by the adenohypophysis (pituitary gland, anterior).

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (734 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

A lactogenic hormone secreted by the adenohypophysis (pituitary gland, anterior). It is a polypeptide of approximately 23 kD. Besides its major action on lactation, in some species prolactin exerts effects on reproduction, maternal behavior, fat metabolism, immunomodulation and osmoregulation. Prolactin receptors are present in the mammary gland, hypothalamus, liver, ovary, testis, and prostate.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Lactogenic Hormone, Pituitary; Hormone, Pituitary Lactogenic; Pituitary Lactogenic Hormone; Mammotropic Hormone, Pituitary; Hormone, Pituitary Mammotropic; Pituitary Mammotropic Hormone; Mammotropin; PRL (Prolactin).

Where it fits in the MeSH classification

Broader topics
Gonadotropins, Pituitary; Pituitary Hormones, Anterior
See also
Hyperprolactinemia; Receptors, Prolactin

Related concepts

  • Pituitary Gland
  • Anterior

Research landscape

PubMed indexes 41,128 records tagged with the MeSH heading “Prolactin” (counts retrieved 2026-10-31). 1,758 of them (4.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 30,552 records.

Reviews account for 2,988 records (7.3%) and meta-analyses for 90. Randomized controlled trials number 1,178 (2.9%) as a share of all records on the topic.

PubMed records by publication periodthrough 1999: 30,552 records; 2000-2009: 5,487 records; 2010-2019: 3,331 records; 2020 onward: 1,758 records30,552through 19995,4872000-20093,3312010-20191,7582020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 199930,552
2000-20095,487
2010-20193,331
2020 onward1,758
Share of records by publication typeReviews: 7.3 percent; Meta-analyses: 0.2 percent; Randomized controlled trials: 2.9 percentReviews7.3% (2,988)Meta-analyses0.2% (90)Randomized controlled trials2.9% (1,178)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 41,128 PubMed records
TypeRecordsShare
Reviews2,9887.3%
Meta-analyses900.2%
Randomized controlled trials1,1782.9%

Method: PubMed query "Prolactin"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.

Reading the evidence in drugs and chemicals

Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Prolactin and Autoimmunity
Borba VV, Zandman-Goddard G, Shoenfeld Y
2018Review article
Design not recorded in structured metadata
161cc by
PMID 29483903 · DOI · PMC5816039
Hormonal Effects on Hair Follicles
Grymowicz M, Rudnicka E, Podfigurna A, Napierala P, Smolarczyk R, Smolarczyk K, et al.
2020Review article
Design not recorded in structured metadata
144cc by
PMID 32731328 · DOI · PMC7432488
Important Hormones Regulating Lipid Metabolism
Zhang D, Wei Y, Huang Q, Chen Y, Zeng K, Yang W, et al.
2022Review article
Design not recorded in structured metadata
89cc by
PMID 36296646 · DOI · PMC9607181
Stress-Induced Activation of Prolactin-NR4A1-Midkine Axis Exacerbates Skin Inflammation
Li Z, Quan H, Liu W, Chen J, Chu M, Tang X, et al.
2026Research article
Design not recorded in structured metadata
5cc by
PMID 41194398 · DOI · PMC12850390

Prolactin and Autoimmunity [1]

Review article Borba VV, Zandman-Goddard G, Shoenfeld Y · · 2018 · cited 161 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The great asymmetry of autoimmune diseases between genders represents one of the most enigmatic observations among the mosaic of autoimmunity.
Closing excerpt
In this review, we attempt to provide a critical overview of the link between PRL, autoimmune diseases, and motherhood.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (222 words)

The great asymmetry of autoimmune diseases between genders represents one of the most enigmatic observations among the mosaic of autoimmunity. Sex hormones are believed to play a crucial role on this dimorphism. The higher prevalence of autoimmunity among women at childbearing ages, disease onset/relapses during pregnancy, and post-partum are some of the arguments that support this hypothesis. Certainly, motherhood represents one of the most remarkable challenges for the immune system, which not only has to allow for the conceptus, but also has to deal with complex endocrine alterations. Hormonal homeostasis is known to exert a crucial influence in achieving a competent and healthy immune system. Prolactin (PRL) has a bioactive function acting as a hormone and a cytokine. It interferes with immune system modulation, mainly inhibiting the negative selection of autoreactive B lymphocytes. Likewise, hyperprolactinemia has been described in relation to the pathogenesis and activity of several autoimmune disorders. Dopamine is an effective inhibitor of PRL secretion due to either a direct influence on the hypophysis or stimulation of postsynaptic dopamine receptors in the hypothalamus, arousing the release of the PRL inhibitory factor. Hence, dopamine agonists have proven to offer clinical benefits among autoimmune patients and represent a promising therapy to be explored. In this review, we attempt to provide a critical overview of the link between PRL, autoimmune diseases, and motherhood.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29483903 · DOI · PMC5816039

Hormonal Effects on Hair Follicles [2]

Review article Grymowicz M, Rudnicka E, Podfigurna A, Napierala P, Smolarczyk R, Smolarczyk K, et al. · · 2020 · cited 144 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The hair cycle and hair follicle structure are highly affected by various hormones.
Closing excerpt
Our review includes results from many analyses and provides a comprehensive up-to-date understanding of the subject of the effects of hormonal changes on the hair follicle.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (192 words)

The hair cycle and hair follicle structure are highly affected by various hormones. Androgens-such as testosterone (T); dihydrotestosterone (DHT); and their prohormones, dehydroepiandrosterone sulfate (DHEAS) and androstendione (A)-are the key factors in terminal hair growth. They act on sex-specific areas of the body, converting small, straight, fair vellus hairs into larger darker terminal hairs. They bind to intracellular androgen receptors in the dermal papilla cells of the hair follicle. The majority of hair follicles also require the intracellular enzyme 5-alpha reductase to convert testosterone into DHT. Apart from androgens, the role of other hormones is also currently being researched-e.g., estradiol can significantly alter the hair follicle growth and cycle by binding to estrogen receptors and influencing aromatase activity, which is responsible for converting androgen into estrogen (E2). Progesterone, at the level of the hair follicle, decreases the conversion of testosterone into DHT. The influence of prolactin (PRL) on hair growth has also been intensively investigated, and PRL and PRL receptors were detected in human scalp skin. Our review includes results from many analyses and provides a comprehensive up-to-date understanding of the subject of the effects of hormonal changes on the hair follicle.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32731328 · DOI · PMC7432488

Important Hormones Regulating Lipid Metabolism [3]

Review article Zhang D, Wei Y, Huang Q, Chen Y, Zeng K, Yang W, et al. · · 2022 · cited 89 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
There is a wide variety of kinds of lipids, and complex structures which determine the diversity and complexity of their functions.
Closing excerpt
Manipulation of hormonal action has the potential to offer a new therapeutic horizon for the global burden of obesity and its associated complications such as morbidity and mortality.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (178 words)

There is a wide variety of kinds of lipids, and complex structures which determine the diversity and complexity of their functions. With the basic characteristic of water insolubility, lipid molecules are independent of the genetic information composed by genes to proteins, which determine the particularity of lipids in the human body, with water as the basic environment and genes to proteins as the genetic system. In this review, we have summarized the current landscape on hormone regulation of lipid metabolism. After the well-studied PI3K-AKT pathway, insulin affects fat synthesis by controlling the activity and production of various transcription factors. New mechanisms of thyroid hormone regulation are discussed, receptor α and β may mediate different procedures, the effect of thyroid hormone on mitochondria provides a new insight for hormones regulating lipid metabolism. Physiological concentration of adrenaline induces the expression of extrapituitary prolactin in adipose tissue macrophages, which promotes fat weight loss. Manipulation of hormonal action has the potential to offer a new therapeutic horizon for the global burden of obesity and its associated complications such as morbidity and mortality.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36296646 · DOI · PMC9607181

Stress-Induced Activation of Prolactin-NR4A1-Midkine Axis Exacerbates Skin Inflammation [4]

Research article Li Z, Quan H, Liu W, Chen J, Chu M, Tang X, et al. · · 2026 · cited 5 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Stress is an established trigger of skin inflammation and disease flares; however, the mechanisms have remained unclear.
Closing excerpt
These data provide a novel mechanism for stress-related amplification of skin inflammation and identify NR4A1 and midkine as potential therapeutic targets to mitigate stress-exacerbated inflammation.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)

Stress is an established trigger of skin inflammation and disease flares; however, the mechanisms have remained unclear. Here, using human data, mechanistic exploration, and single-cell RNA sequencing in mouse models of skin inflammation under stress challenge, prolactin is identified as a key mediator linking stress to inflammatory responses in the skin through an NR4A1-midkine axis in APCDD1+ fibroblasts in the upper dermis. The data shows that prolactin is increased in the plasma of psoriasis patients with high levels of stress and in stressed mice, which activates transcription factor NR4A1 in APCDD1+ fibroblasts, promoting secretion of midkine, and amplification of immune infiltration and responses in neighboring cells. Targeting NR4A1 or midkine effectively reverses these inflammatory effects in vivo. These data provide a novel mechanism for stress-related amplification of skin inflammation and identify NR4A1 and midkine as potential therapeutic targets to mitigate stress-exacerbated inflammation.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41194398 · DOI · PMC12850390

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Prolactin and dopamine: what is the connection? A review article [5]
    Fitzgerald P, Dinan TG · J Psychopharmacol · 2008 · cited 254 times (Europe PMC)
  • Research article The prolactin and growth hormone families: pregnancy-specific hormones/cytokines at the maternal-fetal interface [6]
    Soares MJ · Reprod Biol Endocrinol · 2004 · cited 210 times (Europe PMC)
  • Research article Prolactin - a pleiotropic factor in health and disease [7]
    Bernard V, Young J, Binart N · Nat Rev Endocrinol · 2019 · cited 194 times (Europe PMC)
  • Research article Elevated prolactin levels in patients with schizophrenia: mechanisms and related adverse effects [8]
    Halbreich U, Kinon BJ, Gilmore JA, Kahn LS · Psychoneuroendocrinology · 2003 · cited 158 times (Europe PMC)
  • Research article Prolactin and autoimmunity [9]
    Shelly S, Boaz M, Orbach H · Autoimmun Rev · 2012 · cited 139 times (Europe PMC)
  • Research article Medication-induced hyperprolactinemia [10]
    Molitch ME · Mayo Clin Proc · 2005 · cited 138 times (Europe PMC)

References

  1. Borba VV, Zandman-Goddard G, Shoenfeld Y. Prolactin and Autoimmunity. . 2018. PMID 29483903 · DOI · PMC5816039
  2. Grymowicz M, Rudnicka E, Podfigurna A, Napierala P, Smolarczyk R, Smolarczyk K, et al.. Hormonal Effects on Hair Follicles. . 2020. PMID 32731328 · DOI · PMC7432488
  3. Zhang D, Wei Y, Huang Q, Chen Y, Zeng K, Yang W, et al.. Important Hormones Regulating Lipid Metabolism. . 2022. PMID 36296646 · DOI · PMC9607181
  4. Li Z, Quan H, Liu W, Chen J, Chu M, Tang X, et al.. Stress-Induced Activation of Prolactin-NR4A1-Midkine Axis Exacerbates Skin Inflammation. . 2026. PMID 41194398 · DOI · PMC12850390
  5. Fitzgerald P, Dinan TG. Prolactin and dopamine: what is the connection? A review article. J Psychopharmacol. 2008. PMID 18477617 · DOI
  6. Soares MJ. The prolactin and growth hormone families: pregnancy-specific hormones/cytokines at the maternal-fetal interface. Reprod Biol Endocrinol. 2004. PMID 15236651 · DOI · PMC471570
  7. Bernard V, Young J, Binart N. Prolactin - a pleiotropic factor in health and disease. Nat Rev Endocrinol. 2019. PMID 30899100 · DOI
  8. Halbreich U, Kinon BJ, Gilmore JA, Kahn LS. Elevated prolactin levels in patients with schizophrenia: mechanisms and related adverse effects. Psychoneuroendocrinology. 2003. PMID 12504072 · DOI
  9. Shelly S, Boaz M, Orbach H. Prolactin and autoimmunity. Autoimmun Rev. 2012. PMID 22155203 · DOI
  10. Molitch ME. Medication-induced hyperprolactinemia. Mayo Clin Proc. 2005. PMID 16092584 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-31.

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At a glance

41,128
PubMed records on this heading
4%
published since 2020
2,988
review articles
1,178
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

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