Cited by 227Regulation of Appetite and ObesityNeuroendocrine regulation and behaviorNeuropeptides and Animal Physiology

The DOI matches its Crossref record; 54 of the 55 references it cites were found in a registry or an index; none of the 52 sources its claims cite is checked for support yet.

Oxytocin Reduces Reward-Driven Food Intake in Humans

Open access

Abstract

Experiments in animals suggest that the neuropeptide oxytocin acts as an anorexigenic signal in the central nervous control of food intake. In humans, however, research has almost exclusively focused on the involvement of oxytocin in the regulation of social behavior. We investigated the effect of intranasal oxytocin on ingestion and metabolic function in healthy men. Food intake in the fasted state was examined 45 min after neuropeptide administration, followed by the assessment of olfaction and reward-driven snack intake in the absence of hunger. Energy expenditure was registered by indirect calorimetry, and blood was repeatedly sampled to determine concentrations of blood glucose and hormones. Oxytocin markedly reduced snack consumption, restraining, in particular, the intake of chocolate cookies by 25%. Oxytocin, moreover, attenuated basal and postprandial levels of adrenocorticotropic hormone and cortisol and curbed the meal-related rise in plasma glucose. Energy expenditure and hunger-driven food intake as well as olfactory function were not affected. Our results indicate that oxytocin, beyond its role in social bonding, regulates nonhomeostatic, reward-related energy intake, hypothalamic-pituitary-adrenal axis activity, and the glucoregulatory response to food intake in humans. These effects can be assumed to converge with the psychosocial function of oxytocin and imply possible applications in the treatment of metabolic disorders.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

Intranasal oxytocin (24 IU) in healthy men reduced reward-driven snack intake, especially chocolate cookies, without affecting hunger-driven buffet intake or energy expenditure. It also suppressed HPA-axis activity and blunted the postprandial glucose peak.

Key findings

  • Oxytocin did not affect fasted breakfast-buffet intake or macronutrient proportions (all P > 0.6), but reduced total snack intake in the postprandial period (F1,19 = 5.5, P < 0.03), driven by a 25% decrease in chocolate cookie consumption (P < 0.01).
  • Oxytocin reduced serum ACTH (F1,18 = 4.67, P < 0.05), plasma cortisol (F1,18 = 5.15, P < 0.04), and preprandial norepinephrine (F1,19 = 5.41, P = 0.03); cortisol reduction correlated with reduced chocolate cookie intake (r = 0.56, P = 0.012).
  • The peak plasma glucose response to breakfast was reduced by 0.57 mmol/L after oxytocin vs placebo (P < 0.02), while insulin, C-peptide, total/active GLP-1, ghrelin, leptin, growth hormone, energy expenditure, olfaction, and experimenter trustworthiness were not significantly affected.

Methods

  • Double-blind, placebo-controlled, cross-over within-subject study in 20 healthy, nonsmoking men (aged 26.3 ± 0.89 years; BMI 22.66 ± 0.36 kg/m²), with sessions at least 10 days apart.
  • Participants received intranasal oxytocin (24 IU; six 0.1-mL puffs) or vehicle, then ate ad libitum from a breakfast buffet 45 min later; snack intake was covertly measured 100 min after the buffet under a taste-rating pretext.
  • Analyses used ANOVA with within-subject factors treatment, time, nutrient, and snack type, Greenhouse-Geisser correction, pairwise t tests, baseline adjustment, and ANCOVA for snack intake and glucose peak adjusted for breakfast calorie/carbohydrate intake; P < 0.05 was significant.

Limitations

  • The paper does not include a dedicated limitations section. Evident from the text: the sample was small (n = 20), male, healthy, and normal-weight, so findings may not generalize to women, obese individuals, or clinical populations.
  • Evident from the text: only acute effects of a single 24 IU intranasal dose were tested; long-term effects, weight outcomes, and mechanisms (e.g., VTA/nucleus accumbens dopamine signaling) remain speculative and require corroboration.
  • Evident from the text: snack intake was assessed under a taste-test pretext, although the authors report checks for demand characteristics and experimenter trustworthiness.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.2337/db13-0663

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

0 of 52 cited sources checked · 0 supported · 0 flagged

Show all 57 claims

  • It may state two separate claims as one. 15
  • Probably not a substantial claim. 20
  • The quote only partly states this claim. 1
32 of 32
  • The paper relies on this without support.

    The effect of intranasal oxytocin on energy metabolism, including ingestive behavior, has not been investigated in humans.

    “Surprisingly, however, the effect of intranasal oxytocin on energy metabolism, including ingestive behavior, has not been investigated in humans so far.”
  • The paper relies on this without support.

    In the postprandial period, reward-driven eating motivation prevails.

    “The anorexigenic effect of oxytocin emerged during the postprandial period, when reward-driven eating motivation prevails, whereas energy intake in the fasted state was not affected.”
  • The authors state this as an assumption.

    Opioidergic/cannabinoid signaling processes the palatability of ingested nutrients.

    “Oxytocin did not affect the rated palatability of chocolate cookies, which might be taken as an indication that it acted on dopaminergic pathways responding to the incentive salience of food rather than opioidergic/cannabinoid signaling assumed to process the palatability of ingested nutrients (39).”
  • The paper relies on this without support.

    Excessive reward-driven food intake, chronic HPA axis activation, and insulin resistance are key factors in the pathogenesis and maintenance of obesity.

    “Excessive reward-driven food intake, chronic HPA axis activation, and insulin resistance are key factors in the pathogenesis and maintenance of obesity.”
4 of 4

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Breakfast time differs between figure captions and methods

    Minor

    The figure captions place breakfast at 1000-1030 h, whereas the methods place it at 1030-1100 h. The stated 45-minute delay after administration at 0942 h also supports the later start.

  • ACTH and cortisol sample types are reversed

    Minor

    The results describe serum ACTH and plasma cortisol, but the Figure 2 caption identifies plasma ACTH and serum cortisol.

  • Norepinephrine result cites the leptin panel

    Minor

    The norepinephrine result cites Fig. 3F, but the Figure 3 caption identifies panel F as leptin. The Figure 2 caption identifies its panel F as norepinephrine.

3 of 3

Citations

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Metadata

Authors
Ott, V., Finlayson, G., Lehnert, H., Heitmann, B., Heinrichs, M., Born, J., & Hallschmid, M.
Affiliations
  • University of Lübeck (DE)
  • University of Leeds (GB)
  • University of Freiburg (DE)
  • Department of Medical Psychology and Behavioral Neurobiology, University of Tübingen, Tübingen, Germany
  • University of Tübingen (DE)
Corresponding author
Hallschmid, Manfred
Venue
Diabetes
Published
2013-09-17
Volume
62
Issue
10
Pages
3418-3425
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2138122742
Cited by
226
References
55
Citations by year
2026: 5 · 2025: 17 · 2024: 7 · 2023: 9 · 2022: 11 · 2021: 26 · 2020: 22 · 2019: 20 · 2018: 33 · 2017: 25 · 2016: 26 · 2015: 18 · 2014: 6 · 2013: 1
FWCI
9.16
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
  • Research Bank (Australian Catholic University) (submittedVersion)
  • FreiDok plus (Universitätsbibliothek Freiburg) (submittedVersion)
  • Site cant be reached (submittedVersion)
Funders
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (114788)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
oxytocin, dietary intake, snacking, chocolate cookies, hypothalamic-pituitary-adrenal axis, cortisol, ACTH, energy expenditure, blood glucose, olfaction, hunger, anorexigenic peptides, metabolic disorders
MeSH terms
Administration, Intranasal, Adrenocorticotropic Hormone, Adult, Appetite Depressants, Blood Glucose, Calorimetry, Indirect, Eating, Energy Metabolism, Fasting, Humans, Hunger, Hydrocortisone, Hypothalamo-Hypophyseal System, Insulin, Male, Obesity, Oxytocics, Oxytocin, Pituitary-Adrenal System, Reward, Body Mass Index, Postprandial Period, Ghrelin, Snacks

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