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 (616 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 peptide, of about 33 amino acids, secreted by the upper intestinal mucosa and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety.
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: Pancreozymin; Uropancreozymin; CCK-33; Cholecystokinin 33.
Where it fits in the MeSH classification
- Broader topics
- Gastrointestinal Hormones; Peptides
- Narrower topics
- Sincalide
- See also
- Gastrointestinal Agents; Receptors, Cholecystokinin
Related concepts
Research landscape
PubMed indexes 14,067 records tagged with the MeSH heading “Cholecystokinin” (counts retrieved 2026-10-31). 704 of them (5.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 10,020 records.
Reviews account for 1,167 records (8.3%) and meta-analyses for 9. Randomized controlled trials number 361 (2.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 10,020 |
| 2000-2009 | 2,073 |
| 2010-2019 | 1,270 |
| 2020 onward | 704 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,167 | 8.3% |
| Meta-analyses | 9 | 0.1% |
| Randomized controlled trials | 361 | 2.6% |
Method: PubMed query "Cholecystokinin"[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 |
|---|---|---|---|---|
| Appetite controlled by a cholecystokinin nucleus of the solitary tract to hypothalamus neurocircuit | 2016 | Research article Design not recorded in structured metadata | 148 | cc by PMID 26974347 · DOI · PMC4861598 |
| Ligand recognition and G-protein coupling selectivity of cholecystokinin A receptor | 2021 | Research article Design not recorded in structured metadata | 91 | cc by PMID 34556862 · DOI · PMC8604728 |
| Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes | 2020 | Review article Design not recorded in structured metadata | 87 | cc by PMID 32210918 · DOI · PMC7067705 |
| Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41760660 · DOI · PMC13066563 |
Appetite controlled by a cholecystokinin nucleus of the solitary tract to hypothalamus neurocircuit [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The nucleus of the solitary tract (NTS) is a key gateway for meal-related signals entering the brain from the periphery.
- Closing excerpt
- These data identify the functional significance of CCK(NTS) neurons and reveal a sufficient and discrete NTS to hypothalamus circuit controlling appetite.
- 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)
The nucleus of the solitary tract (NTS) is a key gateway for meal-related signals entering the brain from the periphery. However, the chemical mediators crucial to this process have not been fully elucidated. We reveal that a subset of NTS neurons containing cholecystokinin (CCK(NTS)) is responsive to nutritional state and that their activation reduces appetite and body weight in mice. Cell-specific anterograde tracing revealed that CCK(NTS) neurons provide a distinctive innervation of the paraventricular nucleus of the hypothalamus (PVH), with fibers and varicosities in close apposition to a subset of melanocortin-4 receptor (MC4R(PVH)) cells, which are also responsive to CCK. Optogenetic activation of CCK(NTS) axon terminals within the PVH reveal the satiating function of CCK(NTS) neurons to be mediated by a CCK(NTS)→PVH pathway that also encodes positive valence. These data identify the functional significance of CCK(NTS) neurons and reveal a sufficient and discrete NTS to hypothalamus circuit controlling appetite.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26974347 · DOI · PMC4861598
Ligand recognition and G-protein coupling selectivity of cholecystokinin A receptor [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Cholecystokinin A receptor (CCKAR) belongs to family A G-protein-coupled receptors and regulates nutrient homeostasis upon stimulation by cholecystokinin (CCK).
- Closing excerpt
- Our findings provide a framework for understanding G-protein coupling promiscuity by CCKAR and uncover the mechanism of receptor recognition by sulfated CCK-8.
- 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 (144 words)
Cholecystokinin A receptor (CCKAR) belongs to family A G-protein-coupled receptors and regulates nutrient homeostasis upon stimulation by cholecystokinin (CCK). It is an attractive drug target for gastrointestinal and metabolic diseases. One distinguishing feature of CCKAR is its ability to interact with a sulfated ligand and to couple with divergent G-protein subtypes, including Gs, Gi and Gq. However, the basis for G-protein coupling promiscuity and ligand recognition by CCKAR remains unknown. Here, we present three cryo-electron microscopy structures of sulfated CCK-8-activated CCKAR in complex with Gs, Gi and Gq heterotrimers, respectively. CCKAR presents a similar conformation in the three structures, whereas conformational differences in the 'wavy hook' of the Gα subunits and ICL3 of the receptor serve as determinants in G-protein coupling selectivity. Our findings provide a framework for understanding G-protein coupling promiscuity by CCKAR and uncover the mechanism of receptor recognition by sulfated CCK-8.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34556862 · DOI · PMC8604728
Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The structurally-related peptides, gastrin and cholecystokinin (CCK), were originally discovered as humoral stimulants of gastric acid secretion and pancreatic enzyme release, respectively.
- Closing excerpt
- The potential imaging and therapeutic use of these peptides and their derivatives are also summarized.
- 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)
The structurally-related peptides, gastrin and cholecystokinin (CCK), were originally discovered as humoral stimulants of gastric acid secretion and pancreatic enzyme release, respectively. With the aid of methodological advances in biochemistry, immunochemistry, and molecular biology in the past several decades, our concept of gastrin and CCK as simple gastrointestinal hormones has changed considerably. Extensive in vitro and in vivo studies have shown that gastrin and CCK play important roles in several cellular processes including maintenance of gastric mucosa and pancreatic islet integrity, neurogenesis, and neoplastic transformation. Indeed, gastrin and CCK, as well as their receptors, are expressed in a variety of tumor cell lines, animal models, and human samples, and might contribute to certain carcinogenesis. In this review, we will briefly introduce the gastrin and CCK system and highlight the effects of gastrin and CCK in the regulation of cell proliferation and apoptosis in both normal and abnormal conditions. The potential imaging and therapeutic use of these peptides and their derivatives are also summarized.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32210918 · DOI · PMC7067705
Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Pancreatic endocrine-exocrine crosstalk plays a key role in normal physiology and disease and can be altered by host metabolic states, such as obesity.
- Closing excerpt
- These results define endocrine-exocrine CCK signaling as a bona fide driver of obesity-associated PDAC development and uncover avenues to target the endocrine pancreas to subvert exocrine tumorigenesis.
- 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 (160 words)
Pancreatic endocrine-exocrine crosstalk plays a key role in normal physiology and disease and can be altered by host metabolic states, such as obesity. Classically, endocrine islet beta (β) cell secretion of insulin is thought to promote the development of obesity-associated pancreatic adenocarcinoma (PDAC), an exocrine cell-derived tumor. Here, we show that β cell expression of the peptide hormone cholecystokinin (CCK) is necessary and sufficient for obesity-associated PDAC progression in mice and that CCK expression - rather than insulin - correlates strongly with enhanced tumorigenesis. Single-cell RNA-sequencing, in silico latent-space archetypal and trajectory analysis, and experimental lineage tracing in vivo reveal that obesity induces the expansion of postnatal immature β cells, which adapt to express CCK via stress-responsive JNK/cJun signaling. Finally, obesity perturbs CCK-dependent peri-islet exocrine cell transcriptional states and enhances islet-proximal tumor formation. These results define endocrine-exocrine CCK signaling as a bona fide driver of obesity-associated PDAC development and uncover avenues to target the endocrine pancreas to subvert exocrine tumorigenesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41760660 · DOI · PMC13066563
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 Biological actions of cholecystokinin [5]
- 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 [6]
- Research article Cholecystokinin and gastrin receptors [7]
- Research article The neuroendocrine control of appetite: the role of the endogenous opiates, cholecystokinin, TRH, gamma-amino-butyric-acid and the diazepam receptor [8]
- Research article Gastrointestinal satiety signals II. Cholecystokinin [9]
- Research article Cholecystokinin cells [10]
References
- D'Agostino G, Lyons DJ, Cristiano C, Burke LK, Madara JC, Campbell JN, et al.. Appetite controlled by a cholecystokinin nucleus of the solitary tract to hypothalamus neurocircuit. . 2016. PMID 26974347 · DOI · PMC4861598
- Liu Q, Yang D, Zhuang Y, Croll TI, Cai X, Dai A, et al.. Ligand recognition and G-protein coupling selectivity of cholecystokinin A receptor. . 2021. PMID 34556862 · DOI · PMC8604728
- Zeng Q, Ou L, Wang W, Guo DY. Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes. . 2020. PMID 32210918 · DOI · PMC7067705
- Garcia CC, Venkat A, McQuaid DC, Agabiti SS, Tong A, Mathew B, et al.. Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development. . 2026. PMID 41760660 · DOI · PMC13066563
- Crawley JN, Corwin RL. Biological actions of cholecystokinin. Peptides. 1994. PMID 7937354 · DOI
- 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
- Dufresne M, Seva C, Fourmy D. Cholecystokinin and gastrin receptors. Physiol Rev. 2006. PMID 16816139 · DOI
- Morley JE. The neuroendocrine control of appetite: the role of the endogenous opiates, cholecystokinin, TRH, gamma-amino-butyric-acid and the diazepam receptor. Life Sci. 1980. PMID 6774182 · DOI
- Moran TH, Kinzig KP. Gastrointestinal satiety signals II. Cholecystokinin. Am J Physiol Gastrointest Liver Physiol. 2004. PMID 14715515 · DOI
- Liddle RA. Cholecystokinin cells. Annu Rev Physiol. 1997. PMID 9074762 · 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.