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 (738 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
Natural recurring desire for food. Alterations may be induced by appetite depressants or appetite stimulants.
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: Appetites; Appetite Alterations; Alteration, Appetite; Alterations, Appetite; Appetite Alteration.
Where it fits in the MeSH classification
- Broader topics
- Psychophysiology; Hunger
- Narrower topics
- Appetite Regulation
- See also
- Appetite Depressants; Appetite Stimulants; Craving
Related concepts
- Appetite Depressants
- Appetite Stimulants
Research landscape
PubMed indexes 12,538 records tagged with the MeSH heading “Appetite” (counts retrieved 2026-10-31). 2,064 of them (16.5%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 4,080 records.
Reviews account for 2,523 records (20.1%) and meta-analyses for 100. Randomized controlled trials number 1,699 (13.6%) 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 | 3,515 |
| 2000-2009 | 2,879 |
| 2010-2019 | 4,080 |
| 2020 onward | 2,064 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,523 | 20.1% |
| Meta-analyses | 100 | 0.8% |
| Randomized controlled trials | 1,699 | 13.6% |
Method: PubMed query "Appetite"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 |
|---|---|---|---|---|
| Gut-brain communication by distinct sensory neurons differently controls feeding and glucose metabolism | 2021 | Research article Design not recorded in structured metadata | 190 | cc by PMID 34043943 · DOI · PMC8280952 |
| Sequential appetite suppression by oral and visceral feedback to the brainstem | 2023 | Research article Design not recorded in structured metadata | 84 | cc by PMID 37993711 · DOI · PMC10700140 |
| Leptin-activated hypothalamic BNC2 neurons acutely suppress food intake | 2024 | Research article Design not recorded in structured metadata | 83 | cc by PMID 39478220 · DOI · PMC11618066 |
| Tumor-induced orexigenic imbalance lowers protein appetite and drives early organ wasting symptoms | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41792134 · DOI · PMC13086994 |
Gut-brain communication by distinct sensory neurons differently controls feeding and glucose metabolism [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Sensory neurons relay gut-derived signals to the brain, yet the molecular and functional organization of distinct populations remains unclear.
- Closing excerpt
- Thus, distinct gut-innervating sensory neurons differentially control feeding and glucoregulatory neurocircuits and may provide specific targets for metabolic control.
- 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 (150 words)
Sensory neurons relay gut-derived signals to the brain, yet the molecular and functional organization of distinct populations remains unclear. Here, we employed intersectional genetic manipulations to probe the feeding and glucoregulatory function of distinct sensory neurons. We reconstruct the gut innervation patterns of numerous molecularly defined vagal and spinal afferents and identify their downstream brain targets. Bidirectional chemogenetic manipulations, coupled with behavioral and circuit mapping analysis, demonstrated that gut-innervating, glucagon-like peptide 1 receptor (GLP1R)-expressing vagal afferents relay anorexigenic signals to parabrachial nucleus neurons that control meal termination. Moreover, GLP1R vagal afferent activation improves glucose tolerance, and their inhibition elevates blood glucose levels independent of food intake. In contrast, gut-innervating, GPR65-expressing vagal afferent stimulation increases hepatic glucose production and activates parabrachial neurons that control normoglycemia, but they are dispensable for feeding regulation. Thus, distinct gut-innervating sensory neurons differentially control feeding and glucoregulatory neurocircuits and may provide specific targets for metabolic control.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34043943 · DOI · PMC8280952
Sequential appetite suppression by oral and visceral feedback to the brainstem [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The termination of a meal is controlled by dedicated neural circuits in the caudal brainstem.
- Closing excerpt
- These findings reveal that sequential negative feedback signals from the mouth and gut engage distinct circuits in the caudal brainstem, which in turn control elements of feeding behaviour operating on short and long timescales.
- 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 (228 words)
The termination of a meal is controlled by dedicated neural circuits in the caudal brainstem. A key challenge is to understand how these circuits transform the sensory signals generated during feeding into dynamic control of behaviour. The caudal nucleus of the solitary tract (cNTS) is the first site in the brain where many meal-related signals are sensed and integrated1-4, but how the cNTS processes ingestive feedback during behaviour is unknown. Here we describe how prolactin-releasing hormone (PRLH) and GCG neurons, two principal cNTS cell types that promote non-aversive satiety, are regulated during ingestion. PRLH neurons showed sustained activation by visceral feedback when nutrients were infused into the stomach, but these sustained responses were substantially reduced during oral consumption. Instead, PRLH neurons shifted to a phasic activity pattern that was time-locked to ingestion and linked to the taste of food. Optogenetic manipulations revealed that PRLH neurons control the duration of seconds-timescale feeding bursts, revealing a mechanism by which orosensory signals feed back to restrain the pace of ingestion. By contrast, GCG neurons were activated by mechanical feedback from the gut, tracked the amount of food consumed and promoted satiety that lasted for tens of minutes. These findings reveal that sequential negative feedback signals from the mouth and gut engage distinct circuits in the caudal brainstem, which in turn control elements of feeding behaviour operating on short and long timescales.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37993711 · DOI · PMC10700140
Leptin-activated hypothalamic BNC2 neurons acutely suppress food intake [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Leptin is an adipose tissue hormone that maintains homeostatic control of adipose tissue mass by regulating the activity of specific neural populations controlling appetite and metabolism1.
- Closing excerpt
- These data indicate that BNC2-expressing neurons are a key component of the neural circuit that maintains energy balance, thus filling an important gap in our understanding of the regulation of food intake and leptin action.
- 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 (210 words)
Leptin is an adipose tissue hormone that maintains homeostatic control of adipose tissue mass by regulating the activity of specific neural populations controlling appetite and metabolism1. Leptin regulates food intake by inhibiting orexigenic agouti-related protein (AGRP) neurons and activating anorexigenic pro-opiomelanocortin (POMC) neurons2. However, whereas AGRP neurons regulate food intake on a rapid time scale, acute activation of POMC neurons has only a minimal effect3-5. This has raised the possibility that there is a heretofore unidentified leptin-regulated neural population that rapidly suppresses appetite. Here we report the discovery of a new population of leptin-target neurons expressing basonuclin 2 (Bnc2) in the arcuate nucleus that acutely suppress appetite by directly inhibiting AGRP neurons. Opposite to the effect of AGRP activation, BNC2 neuronal activation elicited a place preference indicative of positive valence in hungry but not fed mice. The activity of BNC2 neurons is modulated by leptin, sensory food cues and nutritional status. Finally, deleting leptin receptors in BNC2 neurons caused marked hyperphagia and obesity, similar to that observed in a leptin receptor knockout in AGRP neurons. These data indicate that BNC2-expressing neurons are a key component of the neural circuit that maintains energy balance, thus filling an important gap in our understanding of the regulation of food intake and leptin action.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39478220 · DOI · PMC11618066
Tumor-induced orexigenic imbalance lowers protein appetite and drives early organ wasting symptoms [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Cancer cachexia (CC) is characterized by organ wasting and ensuing involuntary weight loss.
- Closing excerpt
- Altogether, we provide evidence for an early orexigenic brain imbalance causing low protein appetite that regulates the onset and outcome of organ wasting.
- 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 (150 words)
Cancer cachexia (CC) is characterized by organ wasting and ensuing involuntary weight loss. Despite advances, underlying mechanisms initiating CC remain unclear, including early symptoms like anorexia. Here, we use a fly gut-tumor model with a precise time-window before organ wasting starts. We show that tumor-induced factors involved in inflammation (unpaired 3/ Interleukin-6-like) and reduced insulin signaling (ImpL2/ Insulin Growth Factor Binding Protein) decrease NPF (Neuropeptide F/ Neuropeptide Y) in the brain prior to organ wasting. This early NPF decrease triggers low protein-specific food appetite and anorexia. We find that ImpL2 reduces NPF signaling while upd3 helps by concurrently affecting the blood brain barrier. Tumor-induced NPF decrease, and early reduction of protein appetite drive the onset of weight loss and exacerbate the risk of death during organ wasting. Altogether, we provide evidence for an early orexigenic brain imbalance causing low protein appetite that regulates the onset and outcome of organ wasting.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41792134 · DOI · PMC13086994
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 Hypothalamic circuits regulating appetite and energy homeostasis: pathways to obesity [5]
- Research article Toward a Wiring Diagram Understanding of Appetite Control [6]
- Research article Anorexia of Aging: Risk Factors, Consequences, and Potential Treatments [7]
- Research article Effects of GLP-1 on appetite and weight [8]
- Research article Three Pillars for the Neural Control of Appetite [9]
- Research article Do ketogenic diets really suppress appetite? A systematic review and meta-analysis [10]
References
- Borgmann D, Ciglieri E, Biglari N, Brandt C, Cremer AL, Backes H, et al.. Gut-brain communication by distinct sensory neurons differently controls feeding and glucose metabolism. . 2021. PMID 34043943 · DOI · PMC8280952
- Ly T, Oh JY, Sivakumar N, Shehata S, La Santa Medina N, Huang H, et al.. Sequential appetite suppression by oral and visceral feedback to the brainstem. . 2023. PMID 37993711 · DOI · PMC10700140
- Tan HL, Yin L, Tan Y, Ivanov J, Plucinska K, Ilanges A, et al.. Leptin-activated hypothalamic BNC2 neurons acutely suppress food intake. . 2024. PMID 39478220 · DOI · PMC11618066
- Petsakou A, Filine E, Li M, Chen Y, Zheng A, Perrimon N. Tumor-induced orexigenic imbalance lowers protein appetite and drives early organ wasting symptoms. . 2026. PMID 41792134 · DOI · PMC13086994
- Timper K, Brüning JC. Hypothalamic circuits regulating appetite and energy homeostasis: pathways to obesity. Dis Model Mech. 2017. PMID 28592656 · DOI · PMC5483000
- Andermann ML, Lowell BB. Toward a Wiring Diagram Understanding of Appetite Control. Neuron. 2017. PMID 28817798 · DOI · PMC5657399
- Landi F, Calvani R, Tosato M, Martone AM, Ortolani E, Savera G, et al.. Anorexia of Aging: Risk Factors, Consequences, and Potential Treatments. Nutrients. 2016. PMID 26828516 · DOI · PMC4772033
- Shah M, Vella A. Effects of GLP-1 on appetite and weight. Rev Endocr Metab Disord. 2014. PMID 24811133 · DOI · PMC4119845
- Sternson SM, Eiselt AK. Three Pillars for the Neural Control of Appetite. Annu Rev Physiol. 2017. PMID 27912679 · DOI
- Gibson AA, Seimon RV, Lee CM, Ayre J, Franklin J, Markovic TP, et al.. Do ketogenic diets really suppress appetite? A systematic review and meta-analysis. Obes Rev. 2015. PMID 25402637 · 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.