Peptide YY (PYY): A Short Course on What the Published Studies Report

Course overview

Peptide YY, usually abbreviated PYY, is a 36-amino-acid peptide released from enteroendocrine cells of the distal gut in response to a meal. It belongs to the same structural family as neuropeptide Y and pancreatic polypeptide and signals through Y-family receptors. In the research literature it is most often discussed as a post-prandial satiety signal, but published studies also describe PYY in contexts that have little to do with appetite: host defence in the small intestine, viral transcription in liver cell models, blood vessel biology, tumour and inflammation models, and vomiting responses to a food-borne toxin.

This page walks through those literatures in modules. It describes what researchers measured and what they reported, and nothing more. This page is for educational purposes only and is not medical advice; consult a licensed physician for any questions about health, diagnosis, or treatment. No administration schedules, quantities, or protocols are provided here, because the verified papers summarised below are observational, mechanistic, or animal studies rather than human dosing trials.

What peptide YY is in the published literature

PYY is produced by enteroendocrine L-cells, which are concentrated in the ileum and colon and which also produce glucagon-like peptide-1. A 2022 review in Handbook of Experimental Pharmacology placed PYY within the broader enteroendocrine system and discussed how gut hormone signalling is altered in obesity (PMID 35419621). That review framed the enteroendocrine cell population as a distributed sensory organ that converts nutrient arrival in the gut lumen into hormonal signals reaching the brain, pancreas, and periphery (PMID 35419621).

PYY(1-36) and PYY(3-36)

Two circulating forms are commonly distinguished in the literature. The full-length peptide, PYY(1-36), is cleaved by dipeptidyl peptidase-4 to PYY(3-36), the form that human studies most often measure when they are interested in satiety signalling. A 2020 study in European Journal of Nutrition specifically assayed PYY(3-36) concentrations in women with acute anorexia nervosa and in women described as long-term recovered, illustrating how investigators isolate this fragment when they want a marker of post-prandial appetite signalling (PMID 32166384).

Module 1: PYY in appetite and energy balance research

The most familiar framing of PYY is as a meal-terminating and meal-spacing signal. A 2017 study in Hormones and Behavior examined meal microstructure in mice and reported that PYY induced meal patterns characteristic of aged animals, linking the hormone to the way individual eating bouts are shaped rather than only to total intake (PMID 28916138). That kind of meal-pattern analysis — counting bouts, bout size, and the interval between them — is a standard rodent method for separating a genuine satiety effect from simple malaise or sedation, and the study used it to characterise how PYY reorganised feeding behaviour (PMID 28916138).

In humans, PYY is usually studied as one of several hormones measured alongside metabolic outcomes. A 2015 paper in the British Journal of Nutrition compared lean and obese dietary phenotypes and examined differences in energy and substrate metabolism together with appetite measures, an approach that treats appetite hormones as part of a wider metabolic profile rather than as a single explanatory variable (PMID 26382929). Researchers using this phenotype-comparison design typically ask whether hormonal and substrate-oxidation differences track with self-reported hunger and fullness, and the study reported on these relationships between the phenotype groups (PMID 26382929).

Module 2: PYY and the enteroendocrine system in obesity

Obesity research has repeatedly returned to gut hormones because bariatric surgery changes them dramatically. The 2022 Handbook of Experimental Pharmacology review of the enteroendocrine system in obesity surveyed how L-cell products, including PYY, are considered in the pathophysiology and pharmacology of obesity (PMID 35419621). Reviews of this type are useful for orientation because they place a single hormone in context: PYY does not act alone, and its signal overlaps with GLP-1, ghrelin, cholecystokinin, and vagal afferent input (PMID 35419621).

Importantly, none of the verified papers on this page describe an approved PYY product or a human therapeutic dosing regimen. PYY analogues have been an active area of pharmaceutical interest, but the evidence summarised here does not extend to that literature, and this page does not extrapolate beyond what the cited papers reported.

Module 3: PYY in eating disorders, ageing, and lactation

Anorexia nervosa

The 2020 European Journal of Nutrition study measured PYY(3-36) in acutely ill and long-term recovered anorexia nervosa, a design chosen to ask whether hormonal differences persist after weight restoration or normalise with recovery (PMID 32166384). Comparing an acute state with a long-term recovered state is the central methodological feature of the study, because it distinguishes state markers, which move with current nutritional status, from trait markers, which would remain abnormal after recovery (PMID 32166384).

Ageing and meal structure

Appetite changes with age in many species, and the 2017 mouse work is relevant here because researchers reported that PYY produced meal patterns resembling those of aged mice (PMID 28916138). That observation positions PYY as a candidate contributor to the reduced and restructured feeding seen in ageing rodents rather than as a general appetite suppressant (PMID 28916138).

Lactation

Lactation is a high energy-demand state in which appetite regulation would be expected to shift. A 2015 British Journal of Nutrition study of appetite-regulating hormones during lactation reported increased maternal plasma peptide YY concentrations at 3-6 months postpartum (PMID 26299586). The finding is a descriptive observation in a physiological state, and the study did not test an intervention (PMID 26299586).

Chemotherapy-associated anorexia in animals

Appetite loss during cytotoxic therapy has been modelled in rodents. A 2024 study in Neuropeptides reported that the Japanese herbal formulation ninjinyoeito ameliorated anorexia and altered peptide YY and ghrelin levels in cisplatin-treated mice (PMID 39182332). The relevance for a PYY course is that the study used PYY as a readout of the anorexia state rather than as the administered agent (PMID 39182332).

Module 4: PYY beyond appetite

Gut fungal commensalism

One of the more striking reframings of PYY came from a 2023 Science paper describing peptide YY as a Paneth cell antimicrobial peptide that maintains Candida gut commensalism (PMID 37535745). In that account PYY is not only an endocrine satiety signal but also a host-defence molecule produced in the small intestinal crypt, where researchers reported it helps keep Candida in a commensal rather than invasive state (PMID 37535745).

Hepatitis B virus in cell models

A 2023 paper in Virus Genes reported that peptide YY inhibited transcription and replication of hepatitis B virus by suppressing promoter and enhancer activity (PMID 37380814). This is molecular virology work on viral regulatory elements, and the study describes a mechanism at the level of HBV transcriptional control rather than a clinical outcome in patients (PMID 37380814).

Blood vessels and atherosclerosis

Y-receptor signalling has vascular effects, and a 2015 study in Clinical and Experimental Pharmacology & Physiology examined the role of peptide YY in blood vessel function and atherosclerosis in a rabbit model (PMID 25854545). Rabbit models are used in atherosclerosis research because of their responsiveness to dietary cholesterol, and the study reported on vessel function endpoints in that setting (PMID 25854545).

Tumour growth and inflammation

A 2009 chapter in Methods in Molecular Biology described methods for studying how peptide YY mediates inhibition of tumour growth and inflammation (PMID 19347290). Because it is a methods chapter, its value is largely procedural — it documents assays and models used by researchers investigating anti-proliferative and anti-inflammatory actions of PYY (PMID 19347290). Nothing in that chapter should be read as evidence of a treatment effect in people.

Neuroendocrine tumours as a confounder

Gut and pancreatic neuroendocrine tumours can secrete peptides in ways that complicate interpretation of hormone measurements. A 2025 case report in Endokrynologia Polska described a virilizing insulinoma, an unusual presentation of a pancreatic neuroendocrine tumour (PMID 40728419). The teaching point for a gut-hormone course is that a single abnormal peptide value can reflect tumour biology rather than normal physiology, as the case report illustrated (PMID 40728419).

Module 5: How PYY is measured and why results differ

Several practical issues recur across the literature and explain why PYY findings are often inconsistent between studies:

• Which form is assayed. Total PYY and PYY(3-36) are not interchangeable; the 2020 anorexia nervosa study explicitly reported PYY(3-36) concentrations (PMID 32166384).
• Fasting versus post-prandial sampling. PYY rises after eating, so timing relative to a meal dominates the value obtained, a point emphasised in reviews of enteroendocrine physiology (PMID 35419621).
• Physiological state. Lactation was associated with increased maternal plasma PYY at 3-6 months postpartum in one cohort, showing that life stage matters (PMID 26299586).
• Species and model. Mouse meal-pattern work (PMID 28916138) and rabbit vascular work (PMID 25854545) answer different questions and do not translate directly to humans.
• Pathology. Hormone-secreting neuroendocrine tumours can distort peptide profiles, as in the virilizing insulinoma case report (PMID 40728419).

Peptide YY: What Studies Report

The verified papers collected here are not administration-safety trials, so they do not provide an adverse-event profile for PYY given as a compound. What they do contain are observations relevant to tolerability questions.

The clearest of these concerns nausea and vomiting. A 2023 study in Food and Chemical Toxicology reported that emesis induced by the trichothecene mycotoxin deoxynivalenol and its congeners corresponded to secretion of peptide YY and 5-HT, linking the timing of vomiting to the release of these two gut mediators (PMID 37286030). That study measured endogenous PYY released in response to a toxin rather than PYY given to animals, so it establishes an association between PYY secretion and emesis in that model, not a causal adverse-event rate for any product (PMID 37286030).

A second observation concerns intake suppression itself. Because researchers reported that PYY produced aged-type meal patterns in mice, reduced or restructured feeding is the expected behavioural consequence of elevated PYY signalling in rodents (PMID 28916138). In the cisplatin mouse model, PYY levels changed alongside the anorexia state, again tying the peptide to reduced food intake in illness (PMID 39182332).

A third is that PYY appears to have a homeostatic role in the gut that is not appetite-related: the 2023 Science work described it as a Paneth cell antimicrobial peptide maintaining Candida commensalism, which means altering PYY biology has implications beyond feeding (PMID 37535745).

Study summary table

What this evidence set does not establish

Reading across these papers, several limits are obvious. First, the human studies are observational: they measured PYY in defined groups — lean and obese phenotypes (PMID 26382929), lactating women (PMID 26299586), and women with anorexia nervosa (PMID 32166384) — rather than administering it. Second, the mechanistic and non-appetite findings come from animal, cell, or methods work (PMID 37380814, PMID 25854545, PMID 19347290). Third, none of these papers define human dosing, duration, or safety monitoring, so no such information appears on this page.

Key terms

• L-cell: an enteroendocrine cell of the distal intestine that secretes PYY and GLP-1, described within the enteroendocrine system review (PMID 35419621).
• PYY(3-36): the DPP-4-cleaved fragment assayed in appetite-focused human studies (PMID 32166384).
• Paneth cell: a small-intestinal crypt cell that secretes antimicrobial molecules, and the source of the PYY form described in the 2023 Science report (PMID 37535745).
• Meal pattern analysis: rodent method quantifying bout size and spacing, used to characterise PYY effects in mice (PMID 28916138).

Anyone with questions about gut hormones, appetite, weight, or gastrointestinal symptoms should raise them with a licensed clinician who can evaluate their individual circumstances.

References

• Peptide YY: A Paneth cell antimicrobial peptide that maintains Candida gut commensalism (Science, 2023)
• The Enteroendocrine System in Obesity (Handbook of Experimental Pharmacology, 2022)
• Peptide YY(3-36) concentration in acute- and long-term recovered anorexia nervosa (European Journal of Nutrition, 2020)
• Peptide YY induces characteristic meal patterns of aged mice (Hormones and Behavior, 2017)
• Lean and obese dietary phenotypes: differences in energy and substrate metabolism and appetite (British Journal of Nutrition, 2015)
• Lactation and appetite-regulating hormones: increased maternal plasma peptide YY concentrations 3-6 months postpartum (British Journal of Nutrition, 2015)
• Ninjinyoeito ameliorates anorexia and changes in peptide YY and ghrelin levels of cisplatin-treated mice (Neuropeptides, 2024)
• Role of Peptide YY in blood vessel function and atherosclerosis in a rabbit model (Clinical and Experimental Pharmacology & Physiology, 2015)
• Peptide YY inhibits transcription and replication of hepatitis B virus by suppressing promoter/enhancer activity (Virus Genes, 2023)
• Emesis to trichothecene deoxynivalenol and its congeners correspond to secretion of peptide YY and 5-HT (Food and Chemical Toxicology, 2023)
• Peptide YY mediates inhibition of tumor growth and inflammation (Methods in Molecular Biology, 2009)
• Virilizing insulinoma (Endokrynologia Polska, 2025)