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 (762 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
The middle portion of the small intestine, between duodenum and ileum. It represents about 2/5 of the remaining portion of the small intestine below duodenum.
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: Jejunums.
Where it fits in the MeSH classification
- Broader topics
- Intestine, Small; Lower Gastrointestinal Tract
- See also
- Jejunostomy
Related concepts
Research landscape
PubMed indexes 32,249 records tagged with the MeSH heading “Jejunum” (counts retrieved 2026-10-31). 1,654 of them (5.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 22,659 records.
Reviews account for 914 records (2.8%) and meta-analyses for 39. Randomized controlled trials number 338 (1.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 22,659 |
| 2000-2009 | 3,914 |
| 2010-2019 | 4,022 |
| 2020 onward | 1,654 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 914 | 2.8% |
| Meta-analyses | 39 | 0.1% |
| Randomized controlled trials | 338 | 1.0% |
Method: PubMed query "Jejunum"[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 |
|---|---|---|---|---|
| Human Norovirus Replication in Human Intestinal Enteroids as Model to Evaluate Virus Inactivation | 2018 | Research article Design not recorded in structured metadata | 190 | cc by PMID 30014841 · DOI · PMC6056096 |
| Aging effects on intestinal homeostasis associated with expansion and dysfunction of intestinal epithelial stem cells | 2017 | Research article Design not recorded in structured metadata | 93 | cc by PMID 28854151 · DOI · PMC5611984 |
| Effects of Microcystin-LR on the Microstructure and Inflammation-Related Factors of Jejunum in Mice | 2019 | Research article Design not recorded in structured metadata | 55 | cc by PMID 31438657 · DOI · PMC6783826 |
| A Lysozyme-Derived Peptide Induces GLP-1 Secretion in Mouse Jejunal Organoids and Modulates Glycemia in Rats | 2025 | Research article Design not recorded in structured metadata | 1 | cc by PMID 40528814 · DOI · PMC12232376 |
Human Norovirus Replication in Human Intestinal Enteroids as Model to Evaluate Virus Inactivation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Human noroviruses are a leading cause of epidemic and endemic acute gastroenteritis worldwide and a leading cause of foodborne illness in the United States.
- Closing excerpt
- Taken together, our data confirm the successful replication of human noroviruses in HIEs and their utility as tools to study norovirus inactivation strategies.
- 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)
Human noroviruses are a leading cause of epidemic and endemic acute gastroenteritis worldwide and a leading cause of foodborne illness in the United States. Recently, human intestinal enteroids (HIEs) derived from human small intestinal tissue have been shown to support human norovirus replication. We implemented the HIE system in our laboratory and tested the effect of chlorine and alcohols on human norovirus infectivity. Successful replication was observed for 6 norovirus GII genotypes and was dependent on viral load and genotype of the inoculum. GII.4 viruses had higher replication levels than other genotypes. Regardless of concentration or exposure time, alcohols slightly reduced, but did not completely inactivate, human norovirus. In contrast, complete inactivation of the 3 GII.4 viruses occurred at concentrations as low as 50 ppm of chlorine. Taken together, our data confirm the successful replication of human noroviruses in HIEs and their utility as tools to study norovirus inactivation strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30014841 · DOI · PMC6056096
Aging effects on intestinal homeostasis associated with expansion and dysfunction of intestinal epithelial stem cells [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Intestinal epithelial stem cells (IESCs) are critical to maintain intestinal epithelial function and homeostasis.
- Closing excerpt
- These findings provide new, direct evidence for aging associated IESC dysfunction, and define potential biomarkers and targets for translational studies to assess and maintain IESC function during aging.
- 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 (199 words)
Intestinal epithelial stem cells (IESCs) are critical to maintain intestinal epithelial function and homeostasis. We tested the hypothesis that aging promotes IESC dysfunction using old (18-22 months) and young (2-4 month) Sox9-EGFP IESC reporter mice. Different levels of Sox9-EGFP permit analyses of active IESC (Sox9-EGFPLow), activatable reserve IESC and enteroendocrine cells (Sox9-EGFPHigh), Sox9-EGFPSublow progenitors, and Sox9-EGFPNegative differentiated lineages. Crypt-villus morphology, cellular composition and apoptosis were measured by histology. IESC function was assessed by crypt culture, and proliferation by flow cytometry and histology. Main findings were confirmed in Lgr5-EGFP and Lgr5-LacZ mice. Aging-associated gene expression changes were analyzed by Fluidigm mRNA profiling. Crypts culture from old mice yielded fewer and less complex enteroids. Histology revealed increased villus height and Paneth cells per crypt in old mice. Old mice showed increased numbers and hyperproliferation of Sox9-EGFPLow IESC and Sox9-EGFPHigh cells. Cleaved caspase-3 staining demonstrated increased apoptotic cells in crypts and villi of old mice. Gene expression profiling revealed aging-associated changes in mRNAs associated with cell cycle, oxidative stress and apoptosis specifically in IESC. These findings provide new, direct evidence for aging associated IESC dysfunction, and define potential biomarkers and targets for translational studies to assess and maintain IESC function during aging.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28854151 · DOI · PMC5611984
Effects of Microcystin-LR on the Microstructure and Inflammation-Related Factors of Jejunum in Mice [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The increasing cyanobacterial blooms have recently been considered a severe environmental problem.
- Closing excerpt
- Our data demonstrated MC-LR had the potential to cause intestinal toxicity by destroying the microstructure of the jejunum and inducing an inflammatory response in mice, which provided new insight into understanding the prevention and diagnosis of the intestinal diseases caused by MC-LR.
- 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)
The increasing cyanobacterial blooms have recently been considered a severe environmental problem. Microcystin-leucine arginine (MC-LR) is one of the secondary products of cyanobacteria metabolism and most harmful cyanotoxins found in water bodies. Studies show MC-LR negatively affects various human organs when exposed to it. The phenotype of the jejunal chronic toxicity induced by MC-LR has not been well described. The aim of this paper was to investigate the effects of MC-LR on the jejunal microstructure and expression level of inflammatory-related factors in jejunum. Mice were treated with different doses (1, 30, 60, 90 and 120 μg/L) of MC-LR for six months. The microstructure and mRNA expression levels of inflammation-related factors in jejunum were analyzed. Results showed that the microstructure of the jejunum was destroyed and expression levels of inflammation-related factors interleukin (IL)-1β, interleukin (IL)-8, tumor necrosis factor alpha, transforming growth factor-β1 and interleukin (IL)-10 were altered at different MC-LR concentrations. To the best of our knowledge, this is the first study that mice were exposed to a high dose of MC-LR for six months. Our data demonstrated MC-LR had the potential to cause intestinal toxicity by destroying the microstructure of the jejunum and inducing an inflammatory response in mice, which provided new insight into understanding the prevention and diagnosis of the intestinal diseases caused by MC-LR.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31438657 · DOI · PMC6783826
A Lysozyme-Derived Peptide Induces GLP-1 Secretion in Mouse Jejunal Organoids and Modulates Glycemia in Rats [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Protein digestion products promote the release of incretins, such as GLP-1, which regulate glucose homeostasis.
- Closing excerpt
- These findings suggest the potential therapeutic application of some food peptides against type 2 diabetes.
- 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 (197 words)
Protein digestion products promote the release of incretins, such as GLP-1, which regulate glucose homeostasis. Our previous studies demonstrated that the egg white peptide fraction stimulates GLP-1 secretion in STC-1 cells. Here, the GLP-1 secretion induced by the lysozyme-derived peptide 123WIRGCRL129 and six alanine-substituted analogues was evaluated in mouse jejunal organoids, alongside egg white digest and the amino acid phenylalanine (Phe). Phe induced a faster GLP-1 response, but the peptide 123WIRGCRL129 elicited a similar GLP-1 response, although tested at a 20-fold lower concentration. The GLP-1 release in organoids elicited by the peptide was 57.8 ± 5 pM, while Phe reached 43.7 ± 1 pM at 60 min. In STC-1 cells, the peptide induced 667.7 ± 24.2 pM of GLP-1 compared to 416.6 ± 40.1 pM induced by Phe. Results obtained in STC-1 suggested the involvement of ERK- and AMPK-mediated pathways in the GLP-1 secretion induced by the peptide. Oral glucose tolerance tests in Wistar rats after oral administration of 123WIRGCRL129 showed a reduction in glucose levels, while no changes were observed in the group receiving the amino acid mixture at equimolar concentration. These findings suggest the potential therapeutic application of some food peptides against type 2 diabetes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40528814 · DOI · PMC12232376
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 THE LOCALIZATION OF PHOSPHATASE ACTIVITIES AT THE LEVEL OF ULTRASTRUCTURE [5]
- Research article Clinical and pathological spectrum of coeliac disease--active, silent, latent, potential [6]
- Research article Ezetimibe therapy: mechanism of action and clinical update [7]
- Research article Porcine IPEC-J2 intestinal epithelial cells in microbiological investigations [8]
- Research article Human jejunal effective permeability and its correlation with preclinical drug absorption models [9]
- Research article Systematic review and meta-analysis of single-balloon enteroscopy-assisted ERCP in patients with surgically altered GI anatomy [10]
References
- Costantini V, Morantz EK, Browne H, Ettayebi K, Zeng XL, Atmar RL, et al.. Human Norovirus Replication in Human Intestinal Enteroids as Model to Evaluate Virus Inactivation. . 2018. PMID 30014841 · DOI · PMC6056096
- Moorefield EC, Andres SF, Blue RE, Van Landeghem L, Mah AT, Santoro MA, et al.. Aging effects on intestinal homeostasis associated with expansion and dysfunction of intestinal epithelial stem cells. . 2017. PMID 28854151 · DOI · PMC5611984
- Cao L, Huang F, Massey IY, Wen C, Zheng S, Xu S, et al.. Effects of Microcystin-LR on the Microstructure and Inflammation-Related Factors of Jejunum in Mice. . 2019. PMID 31438657 · DOI · PMC6783826
- Vivanco-Maroto SM, López de Las Hazas MC, Herradón E, Girón R, Miralles B, Paniagua N, et al.. A Lysozyme-Derived Peptide Induces GLP-1 Secretion in Mouse Jejunal Organoids and Modulates Glycemia in Rats. . 2025. PMID 40528814 · DOI · PMC12232376
- GOLDFISCHER S, ESSNER E, NOVIKOFF AB. THE LOCALIZATION OF PHOSPHATASE ACTIVITIES AT THE LEVEL OF ULTRASTRUCTURE. J Histochem Cytochem. 1964. PMID 14187314 · DOI
- Ferguson A, Arranz E, O'Mahony S. Clinical and pathological spectrum of coeliac disease--active, silent, latent, potential. Gut. 1993. PMID 8432463 · DOI · PMC1373959
- Phan BA, Dayspring TD, Toth PP. Ezetimibe therapy: mechanism of action and clinical update. Vasc Health Risk Manag. 2012. PMID 22910633 · DOI · PMC3402055
- Brosnahan AJ, Brown DR. Porcine IPEC-J2 intestinal epithelial cells in microbiological investigations. Vet Microbiol. 2012. PMID 22074860 · DOI · PMC3289732
- Lennernäs H. Human jejunal effective permeability and its correlation with preclinical drug absorption models. J Pharm Pharmacol. 1997. PMID 9255703 · DOI
- Inamdar S, Slattery E, Sejpal DV, Miller LS, Pleskow DK, Berzin TM, et al.. Systematic review and meta-analysis of single-balloon enteroscopy-assisted ERCP in patients with surgically altered GI anatomy. Gastrointest Endosc. 2015. PMID 25922248 · 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.