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 (728 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 36-amino acid peptide produced by the L cells of the distal small intestine and colon. Peptide YY inhibits gastric and pancreatic secretion.
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: PYY Peptide; Peptide, PYY.
Where it fits in the MeSH classification
- Broader topics
- Gastrointestinal Hormones; Peptide Hormones
Research landscape
PubMed indexes 2,540 records tagged with the MeSH heading “Peptide YY” (counts retrieved 2026-10-31). 376 of them (14.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 862 records.
Reviews account for 278 records (10.9%) and meta-analyses for 18. Randomized controlled trials number 348 (13.7%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 682 |
| 2000-2009 | 620 |
| 2010-2019 | 862 |
| 2020 onward | 376 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 278 | 10.9% |
| Meta-analyses | 18 | 0.7% |
| Randomized controlled trials | 348 | 13.7% |
Method: PubMed query "Peptide YY"[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.
Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults [1]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectiveThe colonic microbiota ferment dietary fibres, producing short chain fatty acids.
- Closing excerpt
- Trial registration numberNCT00750438.
- 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 (216 words)
ObjectiveThe colonic microbiota ferment dietary fibres, producing short chain fatty acids. Recent evidence suggests that the short chain fatty acid propionate may play an important role in appetite regulation. We hypothesised that colonic delivery of propionate would increase peptide YY (PYY) and glucagon like peptide-1 (GLP-1) secretion in humans, and reduce energy intake and weight gain in overweight adults.DesignTo investigate whether propionate promotes PYY and GLP-1 secretion, a primary cultured human colonic cell model was developed. To deliver propionate specifically to the colon, we developed a novel inulin-propionate ester. An acute randomised, controlled cross-over study was used to assess the effects of this inulin-propionate ester on energy intake and plasma PYY and GLP-1 concentrations. The long-term effects of inulin-propionate ester on weight gain were subsequently assessed in a randomised, controlled 24-week study involving 60 overweight adults.ResultsPropionate significantly stimulated the release of PYY and GLP-1 from human colonic cells. Acute ingestion of 10 g inulin-propionate ester significantly increased postprandial plasma PYY and GLP-1 and reduced energy intake. Over 24 weeks, 10 g/day inulin-propionate ester supplementation significantly reduced weight gain, intra-abdominal adipose tissue distribution, intrahepatocellular lipid content and prevented the deterioration in insulin sensitivity observed in the inulin-control group.ConclusionsThese data demonstrate for the first time that increasing colonic propionate prevents weight gain in overweight adult humans.Trial registration numberNCT00750438.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25500202 · DOI · PMC4680171
SCFAs strongly stimulate PYY production in human enteroendocrine cells [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Peptide-YY (PYY) and Glucagon-Like Peptide-1 (GLP-1) play important roles in the regulation of food intake and insulin secretion, and are of translational interest in the field of obesity and diabetes.
- Closing excerpt
- In summary, this study revealed a strong regulation of PYY production by SCFA that was evident in humans but not mice, and suggests that high fibre diets elevate plasma concentrations of the anorexigenic hormone PYY, both by targeting gene expression and hormone secretion.
- 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 (200 words)
Peptide-YY (PYY) and Glucagon-Like Peptide-1 (GLP-1) play important roles in the regulation of food intake and insulin secretion, and are of translational interest in the field of obesity and diabetes. PYY production is highest in enteroendocrine cells located in the distal intestine, mirroring the sites where high concentrations of short chain fatty acids (SCFAs) are produced by gut microbiota. We show here that propionate and butyrate strongly increased expression of PYY but not GCG in human cell line and intestinal primary culture models. The effect was predominantly attributable to the histone deacetylase inhibitory activity of SCFA and minor, but significant contributions of FFA2 (GPR43). Consistent with the SCFA-dependent elevation of PYY gene expression, we also observed increased basal and stimulated PYY hormone secretion. Interestingly, the transcriptional stimulation of PYY was specific to human-derived cell models and not reproduced in murine primary cultures. This is likely due to substantial differences in PYY gene structure between mouse and human. In summary, this study revealed a strong regulation of PYY production by SCFA that was evident in humans but not mice, and suggests that high fibre diets elevate plasma concentrations of the anorexigenic hormone PYY, both by targeting gene expression and hormone secretion.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29311617 · DOI · PMC5758799
Peptide YY is critical for acylethanolamine receptor Gpr119-induced activation of gastrointestinal mucosal responses [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Peptide YY (PYY) is released following food intake and regulates intestinal function and glucose homeostasis, but the mechanisms underpinning these processes are unclear.
- Closing excerpt
- Taken together, these data demonstrate a previously unrecognized role of PYY in mediating intestinal Gpr119 activity and an associated function in controlling glucose tolerance.
- 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 (149 words)
Peptide YY (PYY) is released following food intake and regulates intestinal function and glucose homeostasis, but the mechanisms underpinning these processes are unclear. Enteroendocrine L cells contain PYY and express the acylethanolamine receptor, Gpr119. Here, we show that Gpr119 activation inhibited epithelial electrolyte secretion in human and mouse colon in a glucose-sensitive manner. Endogenous PYY selectively mediated these effects, since PYY(-/-) mice showed no Gpr119 response, but responses were observed in NPY(-/-) mice. Importantly, Gpr119 responses in wild-type (WT) mouse tissue and human colon were abolished by Y(1) receptor antagonism, but were not enhanced by dipeptidylpeptidase IV blockade, indicating that PYY processing to PYY(3-36) was not important. In addition, Gpr119 agonism reduced glycemic excursions after oral glucose delivery to WT mice but not PYY(-/-) mice. Taken together, these data demonstrate a previously unrecognized role of PYY in mediating intestinal Gpr119 activity and an associated function in controlling glucose tolerance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 20519124 · DOI · PMC2890049
Phascolarctobacterium faecium reduces food intake via PYY signaling, contributing to the mitigation of body weight gain in diet-induced obese mice [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Excess energy intake contributes to adiposity in obesity.
- Closing excerpt
- This study identifies the mode of action of a human intestinal bacterium recently linked to obesity protection, providing valuable insights into host-microbe interactions governing body weight.
- 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 (163 words)
Excess energy intake contributes to adiposity in obesity. We investigated whether the human intestinal bacterium Phascolarctobacterium faecium could prevent obesity via enteroendocrine pathways in a mouse model of diet-induced obesity (DIO). Daily administration of P. faecium (2 × 109 cells/mouse) reduced food intake through the early overproduction of the satiety hormone peptide YY (PYY) compared to untreated DIO mice. Moreover, P. faecium increased the intestinal levels of branched-chain amino acids, which, in turn, stimulated PYY secretion in neuroendocrine cell cultures and also modified gut microbiota composition. A pair-feeding study demonstrated that the anorexigenic effect of P. faecium contributes to its effects in attenuating body weight gain in DIO mice, but that other mechanisms are also involved in its metabolic benefits. Specifically, P. faecium accelerated gut transit and serum lipid clearance, thereby limiting adiposity independently of food intake. This study identifies the mode of action of a human intestinal bacterium recently linked to obesity protection, providing valuable insights into host-microbe interactions governing body weight.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41566927 · DOI · PMC12834159
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 Ghrelin, CCK, GLP-1, and PYY(3-36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB [5]
- Research article Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut-brain axis [6]
- Research article Distribution of pancreatic polypeptide and peptide YY [7]
- Research article Recent developments in our understanding of the physiological role of PP-fold peptide receptor subtypes [8]
- Research article Acute exercise and hormones related to appetite regulation: a meta-analysis [9]
- Research article Peptide YY(1-36) and peptide YY(3-36): Part I. Distribution, release and actions [10]
References
- Chambers ES, Viardot A, Psichas A, Morrison DJ, Murphy KG, Zac-Varghese SE, et al.. Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. . 2015. PMID 25500202 · DOI · PMC4680171
- Larraufie P, Martin-Gallausiaux C, Lapaque N, Dore J, Gribble FM, Reimann F, et al.. SCFAs strongly stimulate PYY production in human enteroendocrine cells. . 2018. PMID 29311617 · DOI · PMC5758799
- Cox HM, Tough IR, Woolston AM, Zhang L, Nguyen AD, Sainsbury A, et al.. Peptide YY is critical for acylethanolamine receptor Gpr119-induced activation of gastrointestinal mucosal responses. . 2010. PMID 20519124 · DOI · PMC2890049
- Bullich-Vilarrubias C, Romaní-Pérez M, López-Almela I, Pomares-Díaz C, Franzin SB, Esposito G, et al.. Phascolarctobacterium faecium reduces food intake via PYY signaling, contributing to the mitigation of body weight gain in diet-induced obese mice. . 2026. PMID 41566927 · DOI · PMC12834159
- Steinert RE, Feinle-Bisset C, Asarian L, Horowitz M, Beglinger C, Geary N. Ghrelin, CCK, GLP-1, and PYY(3-36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB. Physiol Rev. 2017. PMID 28003328 · DOI · PMC6151490
- Holzer P, Reichmann F, Farzi A. Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut-brain axis. Neuropeptides. 2012. PMID 22979996 · DOI · PMC3516703
- Ekblad E, Sundler F. Distribution of pancreatic polypeptide and peptide YY. Peptides. 2002. PMID 11825640 · DOI
- Berglund MM, Hipskind PA, Gehlert DR. Recent developments in our understanding of the physiological role of PP-fold peptide receptor subtypes. Exp Biol Med (Maywood). 2003. PMID 12626767 · DOI
- Schubert MM, Sabapathy S, Leveritt M, Desbrow B. Acute exercise and hormones related to appetite regulation: a meta-analysis. Sports Med. 2014. PMID 24174308 · DOI
- Ballantyne GH. Peptide YY(1-36) and peptide YY(3-36): Part I. Distribution, release and actions. Obes Surg. 2006. PMID 16687037 · 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.