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: 3 complete abstracts (542 words), 9 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 nodular organ in the abdomen that contains a mixture of endocrine glands and exocrine glands. The small endocrine portion consists of the islets OF langerhans secreting a number of hormones into the blood stream. The large exocrine portion (exocrine pancreas) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the duodenum.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
- Broader topics
- Digestive System
- Narrower topics
- Islets of Langerhans; Pancreas, Exocrine; Pancreatic Ducts
- See also
- Pancreatectomy; Pancreaticojejunostomy
Related concepts
- Abdomen
- Endocrine Glands
- Exocrine Glands
- Islets
- Langerhans
- Exocrine Pancreas
- Duodenum
Research landscape
PubMed indexes 143,008 records tagged with the MeSH heading “Pancreas” (counts retrieved 2026-10-31). 17,143 of them (12.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 71,869 records.
Reviews account for 14,952 records (10.5%) and meta-analyses for 484. Randomized controlled trials number 1,320 (0.9%) 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 | 71,869 |
| 2000-2009 | 24,008 |
| 2010-2019 | 29,988 |
| 2020 onward | 17,143 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 14,952 | 10.5% |
| Meta-analyses | 484 | 0.3% |
| Randomized controlled trials | 1,320 | 0.9% |
Method: PubMed query "Pancreas"[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 |
|---|---|---|---|---|
| Pancreatic islet α cell function and proliferation require the arginine transporter SLC7A2 | 2026 | Research article Design not recorded in structured metadata | 15 | cc by PMID 42294887 · DOI · PMC13262736 |
| Deep single-cell decoding of human pancreatic islets reveals T2D β-cell gene expression defects | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41986506 · DOI · PMC13226668 |
| ALDH1L2 regulates reactive oxygen species and acinar-to-ductal metaplasia in the pancreas | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41922744 · DOI · PMC13120998 |
Pancreatic islet α cell function and proliferation require the arginine transporter SLC7A2 [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Interrupting glucagon signaling decreases gluconeogenesis and the fractional extraction of amino acids by liver from blood, resulting in lower glycemia.
- Closing excerpt
- Together, these data indicate a central role for SLC7A2 in amino acid-stimulated α cell proliferation and islet hormone secretion.
- 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 (202 words)
Interrupting glucagon signaling decreases gluconeogenesis and the fractional extraction of amino acids by liver from blood, resulting in lower glycemia. The resulting hyperaminoacidemia stimulates α cell proliferation and glucagon secretion via a liver/α cell axis. We hypothesized that α cells detect and respond to circulating amino acids' levels via a unique amino acid transporter repertoire. We found that Slc7a2/SLC7A2 is the most highly expressed cationic amino acid transporter in α cells, with its expression being 3-fold greater in α than β cells in both mouse and human. Employing cell culture, zebrafish, and knockout mouse models, we found that the cationic amino acid arginine and SLC7A2 are required for α cell proliferation in response to interrupted glucagon signaling. Ex vivo and in vivo assessment of islet function in Slc7a2-/- mice showed decreased arginine-stimulated glucagon and insulin secretion. We found that arginine activation of mTOR signaling and induction of the glutamine transporter SLC38A5 was dependent on SLC7A2, showing that the role of both in α cell proliferation is dependent on arginine transport and SLC7A2. Finally, we identified single nucleotide polymorphisms in SLC7A2 associated with HbA1c. Together, these data indicate a central role for SLC7A2 in amino acid-stimulated α cell proliferation and islet hormone secretion.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42294887 · DOI · PMC13262736
Deep single-cell decoding of human pancreatic islets reveals T2D β-cell gene expression defects [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Pancreatic islets maintain glucose homeostasis through coordinated action of endocrine and affiliate cell types and are central to type 2 diabetes (T2D) genetics and pathophysiology.
- Closing excerpt
- Together, this genomic resource provides an enhanced type 2 diabetes expression-atlas for data exploration, analysis, and hypothesis testing, as well as a novel genomic resource for insights into T2D pathophysiology and human islet dysfunction.
- 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 (183 words)
Pancreatic islets maintain glucose homeostasis through coordinated action of endocrine and affiliate cell types and are central to type 2 diabetes (T2D) genetics and pathophysiology. Our understanding of robust human islet cell type-specific alterations in T2D remains limited. Here, we report comprehensive single-cell transcriptome profiling of 245,878 human islet cells from 48 donors spanning non-diabetic, pre-diabetic, and T2D states, and we identify 14 distinct cell types detected in every donor. Cell-cluster analysis reveals ~25-30% β-cell reductions consisting of β-cell loss and proportional increases in a senescent β-cell subpopulation in T2D donors, consistent with previous reports. Further, comparative data integration identifies 511 differentially expressed genes (DEGs) in T2D β-cells, including T2D-associated vitamin A metabolism genes, which are linked to impaired β-cell viability by multimodal functional validation. Integration with T2D genetic, proteomic, and mouse model metabolic phenotypes nominates 58 candidate causal T2D genes, including PDZK1 and GRAMD2B, which preserve β-cell mass. Together, this genomic resource provides an enhanced type 2 diabetes expression-atlas for data exploration, analysis, and hypothesis testing, as well as a novel genomic resource for insights into T2D pathophysiology and human islet dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41986506 · DOI · PMC13226668
ALDH1L2 regulates reactive oxygen species and acinar-to-ductal metaplasia in the pancreas [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Acinar-to-ductal metaplasia (ADM) contributes to pancreatic repair after injury1.
- Closing excerpt
- Overall, our findings identify ROS as a driver of ADM and suggest that circulating formate may serve as a biomarker for PDAC progression.
- 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 (157 words)
Acinar-to-ductal metaplasia (ADM) contributes to pancreatic repair after injury1. However, persistent ADM, combined with KRAS mutation, leads to the development of precancerous pancreatic intraepithelial neoplasia (PanIN) that can progress into pancreatic ductal adenocarcinoma (PDAC)2. While PDAC development is well documented, the metabolic rewiring that occurs during early events such as ADM is poorly understood. Here we show that aldehyde dehydrogenase 1 family member L2 (ALDH1L2), an NADPH-producing mitochondrial enzyme of the one-carbon pathway, limits reactive oxygen species (ROS) and formate production in pancreatic acinar cells. However, ALDH1L2 expression decreases progressively during ADM and is completely absent in pancreatic ductal cells. ALDH1L2 loss elevates ROS and promotes ADM in a model of pancreatitis and accelerates tumour progression in models of pancreatic cancer. We also show that formate increases during PDAC progression in mice and humans. Overall, our findings identify ROS as a driver of ADM and suggest that circulating formate may serve as a biomarker for PDAC progression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41922744 · DOI · PMC13120998
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 Arterial resection during pancreatectomy for pancreatic cancer: a systematic review and meta-analysis [4]
- Research article Impact of type 2 diabetes susceptibility variants on quantitative glycemic traits reveals mechanistic heterogeneity [5]
- Research article How good is endoscopic ultrasound-guided fine-needle aspiration in diagnosing the correct etiology for a solid pancreatic mass?: A meta-analysis and systematic review [6]
- Research article Systematic review and meta-analysis of the volume-outcome relationship in pancreatic surgery [7]
- Research article Magnetic resonance cholangiopancreatography: a meta-analysis of test performance in suspected biliary disease [8]
- Research article Ectopic fat accumulation in the pancreas and its clinical relevance: A systematic review, meta-analysis, and meta-regression [9]
References
- Spears E, Stanley JE, Shou M, Yin L, Li X, Dai C, et al.. Pancreatic islet α cell function and proliferation require the arginine transporter SLC7A2. . 2026. PMID 42294887 · DOI · PMC13262736
- Bandesh K, Motakis E, Nargund S, Kursawe R, Selvam V, Ansarullah, et al.. Deep single-cell decoding of human pancreatic islets reveals T2D β-cell gene expression defects. . 2026. PMID 41986506 · DOI · PMC13226668
- Hennequart M, Mervant L, Stockis J, Coomes J, Zarou MM, Gerard L, et al.. ALDH1L2 regulates reactive oxygen species and acinar-to-ductal metaplasia in the pancreas. . 2026. PMID 41922744 · DOI · PMC13120998
- Mollberg N, Rahbari NN, Koch M, Hartwig W, Hoeger Y, Büchler MW, et al.. Arterial resection during pancreatectomy for pancreatic cancer: a systematic review and meta-analysis. Ann Surg. 2011. PMID 22064622 · DOI
- Dimas AS, Lagou V, Barker A, Knowles JW, Mägi R, Hivert MF, et al.. Impact of type 2 diabetes susceptibility variants on quantitative glycemic traits reveals mechanistic heterogeneity. Diabetes. 2014. PMID 24296717 · DOI · PMC4030103
- Puli SR, Bechtold ML, Buxbaum JL, Eloubeidi MA. How good is endoscopic ultrasound-guided fine-needle aspiration in diagnosing the correct etiology for a solid pancreatic mass?: A meta-analysis and systematic review. Pancreas. 2013. PMID 23254913 · DOI
- Gooiker GA, van Gijn W, Wouters MW, Post PN, van de Velde CJ, Tollenaar RA, et al.. Systematic review and meta-analysis of the volume-outcome relationship in pancreatic surgery. Br J Surg. 2011. PMID 21500187 · DOI
- Romagnuolo J, Bardou M, Rahme E, Joseph L, Reinhold C, Barkun AN. Magnetic resonance cholangiopancreatography: a meta-analysis of test performance in suspected biliary disease. Ann Intern Med. 2003. PMID 14530225 · DOI
- Singh RG, Yoon HD, Wu LM, Lu J, Plank LD, Petrov MS. Ectopic fat accumulation in the pancreas and its clinical relevance: A systematic review, meta-analysis, and meta-regression. Metabolism. 2017. PMID 28285638 · 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.