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 (879 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 31-amino acid peptide that is the C-terminal fragment of beta-lipotropin. It acts on opioid receptors and is an analgesic. Its first four amino acids at the N-terminal are identical to the tetrapeptide sequence of methionine enkephalin and leucine enkephalin.
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: beta Endorphin; Endorphin, beta; beta-Endorphin (1-31).
Where it fits in the MeSH classification
- Broader topics
- Pro-Opiomelanocortin; Endorphins
Related concepts
- Beta-Lipotropin
- Opioid Receptors
- Methionine Enkephalin
- Leucine Enkephalin
Research landscape
PubMed indexes 6,559 records tagged with the MeSH heading “beta-Endorphin” (counts retrieved 2026-10-31). 167 of them (2.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 5,098 records.
Reviews account for 333 records (5.1%) and meta-analyses for 2. Randomized controlled trials number 240 (3.7%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 5,098 |
| 2000-2009 | 845 |
| 2010-2019 | 449 |
| 2020 onward | 167 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 333 | 5.1% |
| Meta-analyses | 2 | 0.0% |
| Randomized controlled trials | 240 | 3.7% |
Method: PubMed query "beta-Endorphin"[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 / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Roles of β-Endorphin in Stress, Behavior, Neuroinflammation, and Brain Energy Metabolism | 2020 | Review article Design not recorded in structured metadata | 138 | cc by PMID 33396962 · DOI · PMC7796446 |
| Pain reactivity and plasma beta-endorphin in children and adolescents with autistic disorder | 2009 | Research article Design not recorded in structured metadata | 100 | cc by PMID 19707566 · DOI · PMC2728512 |
| Cannabinoid CB2 receptors contribute to upregulation of β-endorphin in inflamed skin tissues by electroacupuncture | 2011 | Research article Design not recorded in structured metadata | 66 | cc by PMID 22177137 · DOI · PMC3281798 |
| β-Endorphin Mediates Electroacupuncture-Induced Remyelination via Neural Stem Cell Lineage Modulation in Experimental Autoimmune Encephalomyelitis | 2025 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41277766 · DOI · PMC12641445 |
Roles of β-Endorphin in Stress, Behavior, Neuroinflammation, and Brain Energy Metabolism [1]
Abstract reading summary — source excerpts
- Opening excerpt
- β-Endorphins are peptides that exert a wide variety of effects throughout the body.
- Closing excerpt
- This review briefly summarizes the basics of endorphin function, goes over the behaviors and regulatory pathways it governs, and examines the variability of β-endorphin levels observed between normal and disease/disorder affected individuals.
- 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 (130 words)
β-Endorphins are peptides that exert a wide variety of effects throughout the body. Produced through the cleavage pro-opiomelanocortin (POMC), β-endorphins are the primarily agonist of mu opioid receptors, which can be found throughout the body, brain, and cells of the immune system that regulate a diverse set of systems. As an agonist of the body's opioid receptors, β-endorphins are most noted for their potent analgesic effects, but they also have their involvement in reward-centric and homeostasis-restoring behaviors, among other effects. These effects have implicated the peptide in psychiatric and neurodegenerative disorders, making it a research target of interest. This review briefly summarizes the basics of endorphin function, goes over the behaviors and regulatory pathways it governs, and examines the variability of β-endorphin levels observed between normal and disease/disorder affected individuals.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33396962 · DOI · PMC7796446
Pain reactivity and plasma beta-endorphin in children and adolescents with autistic disorder [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundReports of reduced pain sensitivity in autism have prompted opioid theories of autism and have practical care ramifications.
- Closing excerpt
- Clinical care practice and hypotheses regarding underlying mechanisms need to assume that children with autism are sensitive to pain.
- 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 (235 words)
BackgroundReports of reduced pain sensitivity in autism have prompted opioid theories of autism and have practical care ramifications. Our objective was to examine behavioral and physiological pain responses, plasma beta-endorphin levels and their relationship in a large group of individuals with autism.Methodology/principal findingsThe study was conducted on 73 children and adolescents with autism and 115 normal individuals matched for age, sex and pubertal stage. Behavioral pain reactivity of individuals with autism was assessed in three observational situations (parents at home, two caregivers at day-care, a nurse and child psychiatrist during blood drawing), and compared to controls during venepuncture. Plasma beta-endorphin concentrations were measured by radioimmunoassay. A high proportion of individuals with autism displayed absent or reduced behavioral pain reactivity at home (68.6%), at day-care (34.2%) and during venepuncture (55.6%). Despite their high rate of absent behavioral pain reactivity during venepuncture (41.3 vs. 8.7% of controls, PConclusions/significanceThe greater heart rate response to venepuncture and the elevated plasma beta-endorphin found in individuals with autism reflect enhanced physiological and biological stress responses that are dissociated from observable emotional and behavioral reactions. The results suggest strongly that prior reports of reduced pain sensitivity in autism are related to a different mode of pain expression rather than to an insensitivity or endogenous analgesia, and do not support opioid theories of autism. Clinical care practice and hypotheses regarding underlying mechanisms need to assume that children with autism are sensitive to pain.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 19707566 · DOI · PMC2728512
Cannabinoid CB2 receptors contribute to upregulation of β-endorphin in inflamed skin tissues by electroacupuncture [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundElectroacupuncture (EA) can produce analgesia by increasing the β-endorphin level and activation of peripheral μ-opioid receptors in inflamed tissues.
- Closing excerpt
- EA increases endogenous opioid expression in keratinocytes and infiltrating immune cells at the inflammatory site through CB2R activation.
- 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 (281 words)
BackgroundElectroacupuncture (EA) can produce analgesia by increasing the β-endorphin level and activation of peripheral μ-opioid receptors in inflamed tissues. Endogenous cannabinoids and peripheral cannabinoid CB2 receptors (CB2Rs) are also involved in the antinociceptive effect of EA on inflammatory pain. However, little is known about how peripheral CB2Rs interact with the endogenous opioid system at the inflammatory site and how this interaction contributes to the antinociceptive effect of EA on inflammatory pain. In this study, we determined the role of peripheral CB2Rs in the effects of EA on the expression of β-endorphin in inflamed skin tissues and inflammatory pain.ResultsInflammatory pain was induced by injection of complete Freund's adjuvant into the left hindpaw of rats. Thermal hyperalgesia was tested with a radiant heat stimulus, and mechanical allodynia was quantified using von Frey filaments. The mRNA level of POMC and protein level of β-endorphin were quantified by real-time PCR and Western blotting, respectively. The β-endorphin-containing keratinocytes and immune cells in the inflamed skin tissues were detected by double-immunofluorescence labeling. The CB2R agonist AM1241 or EA significantly reduced thermal hyperalgesia and mechanical allodynia, whereas the selective μ-opioid receptor antagonist β-funaltrexamine significantly attenuated the antinociceptive effect produced by them. AM1241 or EA significantly increased the mRNA level of POMC and the protein level of β-endorphin in inflamed skin tissues, and these effects were significantly attenuated by pretreatment with the CB2R antagonist AM630. AM1241 or EA also significantly increased the percentage of β-endorphin-immunoreactive keratinocytes, macrophages, and T-lymphocytes in inflamed skin tissues, and these effects were blocked by AM630.ConclusionsEA and CB2R stimulation reduce inflammatory pain through activation of μ-opioid receptors. EA increases endogenous opioid expression in keratinocytes and infiltrating immune cells at the inflammatory site through CB2R activation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 22177137 · DOI · PMC3281798
β-Endorphin Mediates Electroacupuncture-Induced Remyelination via Neural Stem Cell Lineage Modulation in Experimental Autoimmune Encephalomyelitis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsEffective remyelination in multiple sclerosis (MS) requires both the proliferation of endogenous neural stem cells (NSCs) and their lineage-specific differentiation into oligodendrocyte progenitor cells (OPCs).
- Closing excerpt
- These findings reveal a novel neuroregenerative mechanism and support EA as a promising adjunctive strategy for demyelinating diseases such as MS.
- 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 (233 words)
AimsEffective remyelination in multiple sclerosis (MS) requires both the proliferation of endogenous neural stem cells (NSCs) and their lineage-specific differentiation into oligodendrocyte progenitor cells (OPCs). This study aimed to investigate whether electroacupuncture (EA) promoted NSC proliferation and OPC differentiation via β-endorphin (β-EP)-mediated opioid signaling in a murine model of MS.MethodsExperimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice to model MS. EA stimulation was applied daily at the Zusanli (ST36) acupoint. NSC proliferation and OPC differentiation were assessed via immunofluorescence, flow cytometry (FCM), and RT-qPCR. β-EP expression and opioid receptor involvement were evaluated in the hypothalamus and subventricular zone (SVZ). Naloxone, a nonselective opioid receptor antagonist, was used to determine the role of opioid signaling in EA-induced effects.ResultsEA significantly enhanced NSC proliferation and increased the proportion of NSC-derived OPCs in the SVZ of EAE mice. EA treatment improved clinical score, reduced demyelination, and attenuated leukocyte infiltration of the central nervous system (CNS). Mechanistically, EA upregulated β-EP and its precursor pro-opiomelanocortin (POMC), along with opioid receptors μ-opioid receptor (MOR) and κ-opioid receptor (KOR) (encoded by Oprm1 and Oprk1, respectively). Naloxone administration abolished the beneficial effects of EA on NSC behavior and remyelination, confirming the involvement of opioid receptor-dependent β-EP signaling.ConclusionEA promotes remyelination in EAE mice by stimulating β-EP-mediated NSC proliferation and OPC differentiation. These findings reveal a novel neuroregenerative mechanism and support EA as a promising adjunctive strategy for demyelinating diseases such as MS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41277766 · DOI · PMC12641445
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 Effects of exercise and physical activity on depression [5]
- Research article Beta-endorphin response to exercise. An update [6]
- Research article Changes in beta-endorphin levels in response to aerobic and anaerobic exercise [7]
- Research article Beta-endorphin: cytokine and neuropeptide [8]
- Research article Understanding endorphins and their importance in pain management [9]
- Research article Beta-endorphin and drug-induced reward and reinforcement [10]
References
- Pilozzi A, Carro C, Huang X. Roles of β-Endorphin in Stress, Behavior, Neuroinflammation, and Brain Energy Metabolism. . 2020. PMID 33396962 · DOI · PMC7796446
- Tordjman S, Anderson GM, Botbol M, Brailly-Tabard S, Perez-Diaz F, Graignic R, et al.. Pain reactivity and plasma beta-endorphin in children and adolescents with autistic disorder. . 2009. PMID 19707566 · DOI · PMC2728512
- Su TF, Zhang LH, Peng M, Wu CH, Pan W, Tian B, et al.. Cannabinoid CB2 receptors contribute to upregulation of β-endorphin in inflamed skin tissues by electroacupuncture. . 2011. PMID 22177137 · DOI · PMC3281798
- Wang Y, Ma X, Qiao Z, Zhuang W, Zhang X, Luo J, et al.. β-Endorphin Mediates Electroacupuncture-Induced Remyelination via Neural Stem Cell Lineage Modulation in Experimental Autoimmune Encephalomyelitis. . 2025. PMID 41277766 · DOI · PMC12641445
- Dinas PC, Koutedakis Y, Flouris AD. Effects of exercise and physical activity on depression. Ir J Med Sci. 2011. PMID 21076975 · DOI
- Goldfarb AH, Jamurtas AZ. Beta-endorphin response to exercise. An update. Sports Med. 1997. PMID 9257407 · DOI
- Schwarz L, Kindermann W. Changes in beta-endorphin levels in response to aerobic and anaerobic exercise. Sports Med. 1992. PMID 1553453 · DOI
- Heijnen CJ, Kavelaars A, Ballieux RE. Beta-endorphin: cytokine and neuropeptide. Immunol Rev. 1991. PMID 2045122 · DOI
- Sprouse-Blum AS, Smith G, Sugai D, Parsa FD. Understanding endorphins and their importance in pain management. Hawaii Med J. 2010. PMID 20397507 · PMC3104618
- Roth-Deri I, Green-Sadan T, Yadid G. Beta-endorphin and drug-induced reward and reinforcement. Prog Neurobiol. 2008. PMID 18602444 · 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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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.