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 (514 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
Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the pancreas among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete insulin. Alpha cells (5-20%) secrete glucagon. PP cells (10-35%) secrete pancreatic polypeptide. Delta cells (~5%) secrete somatostatin.
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: Langerhans Islets; Nesidioblasts; Nesidioblast; Pancreas, Endocrine; Endocrine Pancreas; Islet Cells; Cell, Islet; Cells, Islet.
Where it fits in the MeSH classification
- Broader topics
- Pancreas; Endocrine Glands
- Narrower topics
- Glucagon-Secreting Cells; Insulin-Secreting Cells; Pancreatic Polypeptide-Secreting Cells; Somatostatin-Secreting Cells
Related concepts
Research landscape
PubMed indexes 56,254 records tagged with the MeSH heading “Islets of Langerhans” (counts retrieved 2026-10-31). 7,459 of them (13.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 20,992 records.
Reviews account for 7,369 records (13.1%) and meta-analyses for 79. Randomized controlled trials number 680 (1.2%) 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 | 20,992 |
| 2000-2009 | 12,016 |
| 2010-2019 | 15,787 |
| 2020 onward | 7,459 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 7,369 | 13.1% |
| Meta-analyses | 79 | 0.1% |
| Randomized controlled trials | 680 | 1.2% |
Method: PubMed query "Islets of Langerhans"[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 |
|---|---|---|---|---|
| Small things matter: Lack of extraislet β cells in type 1 diabetes | 2025 | Research article Design not recorded in structured metadata | 24 | cc by PMID 41223263 · DOI · PMC12609120 |
| Altered immune and metabolic molecular pathways drive islet cell dysfunction in human type 1 diabetes | 2025 | Research article Design not recorded in structured metadata | 16 | cc by PMID 41026524 · DOI · PMC12646676 |
| 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 |
Small things matter: Lack of extraislet β cells in type 1 diabetes [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Recent three-dimensional (3D) analyses reported an abundance of small β cell-rich endocrine objects (EOs) in the human pancreas.
- Closing excerpt
- This finding has important implications, which will inform future screening and treatment strategies for T1D.
- 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 (128 words)
Recent three-dimensional (3D) analyses reported an abundance of small β cell-rich endocrine objects (EOs) in the human pancreas. Here, we used archival, immunolabeled 2D pancreas sections to assess morphological EO parameters in donors with or without type 1 diabetes (T1D), varying in age and disease duration. We confirm that abundant small, insulin-positive EOs are present in donors without diabetes and comprise most of the pancreatic endocrine area in early life. Small EOs are virtually absent in individuals with T1D, and this effect is most pronounced in children diagnosed with T1D in their earliest years. We conclude that extraislet β cells are affected in T1D development, and their early loss is a characteristic feature. This finding has important implications, which will inform future screening and treatment strategies for T1D.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41223263 · DOI · PMC12609120
Altered immune and metabolic molecular pathways drive islet cell dysfunction in human type 1 diabetes [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Type 1 diabetes (T1D) is characterized by the autoimmune destruction of most insulin-producing β cells, along with dysregulated glucagon secretion from pancreatic α cells.
- Closing excerpt
- These findings underscore the complex interplay between immune signaling, metabolic stress, and cellular identity in shaping islet cell phenotypes in T1D.
- 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 (184 words)
Type 1 diabetes (T1D) is characterized by the autoimmune destruction of most insulin-producing β cells, along with dysregulated glucagon secretion from pancreatic α cells. We conducted an integrated analysis that combines electrophysiological and transcriptomic profiling, along with machine learning, of islet cells from T1D donors. The few surviving β cells exhibit altered electrophysiological properties and transcriptomic signatures indicative of increased antigen presentation, metabolic reprogramming, and impaired protein translation. In α cells, we observed hyperresponsiveness and increased exocytosis, which are associated with upregulated immune signaling, disrupted transcription factor localization, and lysosome homeostasis, as well as dysregulation of mTORC1 complex signaling. Notably, key genetic risk signals for T1D were enriched in transcripts related to α cell dysfunction, including MHC class I, which were closely linked with α cell dysfunction. Our data provide what we believe are novel insights into the molecular underpinnings of islet cell dysfunction in T1D, highlighting pathways that may be leveraged to preserve residual β cell function and modulate α cell activity. These findings underscore the complex interplay between immune signaling, metabolic stress, and cellular identity in shaping islet cell phenotypes in T1D.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41026524 · DOI · PMC12646676
Pancreatic islet α cell function and proliferation require the arginine transporter SLC7A2 [3]
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
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 Diabetes mellitus: Classification, mediators, and complications; A gate to identify potential targets for the development of new effective treatments [4]
- Research article Impact of type 2 diabetes susceptibility variants on quantitative glycemic traits reveals mechanistic heterogeneity [5]
- Research article Inter-organ crosstalk during development and progression of type 2 diabetes mellitus [6]
- Research article Type 1 diabetes [7]
- Research article Developments in stem cell-derived islet replacement therapy for treating type 1 diabetes [8]
- Research article A central role for GRB10 in regulation of islet function in man [9]
References
- Murrall K, Luckett T, Lekka C, Flaxman CS, Wyatt R, Akhbari P, et al.. Small things matter: Lack of extraislet β cells in type 1 diabetes. . 2025. PMID 41223263 · DOI · PMC12609120
- Dos Santos T, Dai XQ, Jones RC, Spigelman AF, Mummey HM, Ewald JD, et al.. Altered immune and metabolic molecular pathways drive islet cell dysfunction in human type 1 diabetes. . 2025. PMID 41026524 · DOI · PMC12646676
- 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
- Antar SA, Ashour NA, Sharaky M, Khattab M, Ashour NA, Zaid RT, et al.. Diabetes mellitus: Classification, mediators, and complications; A gate to identify potential targets for the development of new effective treatments. Biomed Pharmacother. 2023. PMID 37857245 · 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
- Xourafa G, Korbmacher M, Roden M. Inter-organ crosstalk during development and progression of type 2 diabetes mellitus. Nat Rev Endocrinol. 2024. PMID 37845351 · DOI
- Quattrin T, Mastrandrea LD, Walker LSK. Type 1 diabetes. Lancet. 2023. PMID 37030316 · DOI
- Hogrebe NJ, Ishahak M, Millman JR. Developments in stem cell-derived islet replacement therapy for treating type 1 diabetes. Cell Stem Cell. 2023. PMID 37146579 · DOI · PMC10167558
- Prokopenko I, Poon W, Mägi R, Prasad B R, Salehi SA, Almgren P, et al.. A central role for GRB10 in regulation of islet function in man. PLoS Genet. 2014. PMID 24699409 · DOI · PMC3974640
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.