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 (589 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
Peptide hormones that cause an increase in the absorption of glucose by cells within organs such as liver; muscle and adipose tissue. During normal metabolism insulins are produced by the pancreatic beta cells in response to increased glucose. Natural and chemically-modified forms of insulin are also used in the treatment of glucose metabolism disorders such as diabetes mellitus.
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
- Pancreatic Hormones
- Narrower topics
- Biphasic Insulins; Insulin, Long-Acting; Insulin, Short-Acting; Proinsulin
Related concepts
- Glucose
- Liver
- Muscle
- Adipose Tissue
- Pancreatic Beta Cells
- Glucose Metabolism Disorders
- Diabetes Mellitus
Research landscape
PubMed indexes 218,302 records tagged with the MeSH heading “Insulins” (counts retrieved 2026-10-31). 27,784 of them (12.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 96,873 records.
Reviews account for 21,899 records (10.0%) and meta-analyses for 1,470. Randomized controlled trials number 12,490 (5.7%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 96,873 |
| 2000-2009 | 43,768 |
| 2010-2019 | 49,877 |
| 2020 onward | 27,784 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 21,899 | 10.0% |
| Meta-analyses | 1,470 | 0.7% |
| Randomized controlled trials | 12,490 | 5.7% |
Method: PubMed query "Insulins"[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 |
|---|---|---|---|---|
| Lifespan and Fecundity Impacts of Reduced Insulin Signalling Can Be Directed by Mito-Nuclear Epistasis in Drosophila | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41640114 · DOI · PMC12873451 |
| Glucagon promotes net hepatic glycogen repletion following meal ingestion | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41774508 · DOI · PMC13135395 |
| A novel region of the insulin B9-23 sequence is targeted by a HIP-reactive diabetogenic T cell clone | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42591790 · DOI · PMC13462851 |
Lifespan and Fecundity Impacts of Reduced Insulin Signalling Can Be Directed by Mito-Nuclear Epistasis in Drosophila [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The changing demography of human populations has motivated a search for interventions that promote healthy ageing, and especially for evolutionarily-conserved mechanisms that can be studied in lab systems to generate hypotheses about function in humans.
- Closing excerpt
- This suggests that, while insulin signalling has a conserved effect on ageing among species, intraspecific effects can vary genetically, and the combination of mtDNA and nDNA can act as a gatekeeper.
- 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 (185 words)
The changing demography of human populations has motivated a search for interventions that promote healthy ageing, and especially for evolutionarily-conserved mechanisms that can be studied in lab systems to generate hypotheses about function in humans. Reduced Insulin/IGF signalling (IIS) is a leading example, which can extend healthy lifespan in a range of animals, but whether benefits and costs of reduced IIS vary genetically within species is under-studied. This information is critical for any putative translation. Here, in Drosophila, we test for genetic variation in lifespan response to a dominant-negative form of the insulin receptor, along with a metric of fecundity to evaluate corollary fitness costs/benefits. We also partition genetic variation between DNA variants in the nucleus (nDNA) and mitochondrial DNA (mtDNA), in a fully-factorial design that allows us to assess 'mito-nuclear' epistasis. We show that reduced IIS can have either beneficial or detrimental effects on lifespan, depending on the combination of mtDNA and nDNA. This suggests that, while insulin signalling has a conserved effect on ageing among species, intraspecific effects can vary genetically, and the combination of mtDNA and nDNA can act as a gatekeeper.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41640114 · DOI · PMC12873451
Glucagon promotes net hepatic glycogen repletion following meal ingestion [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Insulin and glucagon are described as having opposing actions on hepatic glycogen metabolism.
- Closing excerpt
- Coordinated insulin-glucagon signaling, thus, emerged as a critical mechanism for hepatic glycogen cycling, challenging the classical paradigm that these hormones work in opposition.
- 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)
Insulin and glucagon are described as having opposing actions on hepatic glycogen metabolism. However, here we showed that their coordinated action promoted glycogen turnover and meal glucose storage. In mice, pharmacological doses of insulin or glucagon failed to alter hepatic glycogen, but the combination produced a robust decrease in glycogen content. Additivity between insulin and glucagon was also seen with the activation of hepatic insulin signaling intermediates. This signaling pathway drove glycogen synthesis, suggesting concurrent actions on glycogen breakdown and repletion. A mixed nutrient meal, which stimulates an increase in both insulin and glucagon, enhanced the incorporation of dietary glucose into hepatic glycogen. This was much more pronounced than the effects of glucose alone, which only stimulated insulin secretion. These findings revealed that glucagon is required for efficient hepatic glucose storage when acting in concert with insulin. Coordinated insulin-glucagon signaling, thus, emerged as a critical mechanism for hepatic glycogen cycling, challenging the classical paradigm that these hormones work in opposition.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41774508 · DOI · PMC13135395
A novel region of the insulin B9-23 sequence is targeted by a HIP-reactive diabetogenic T cell clone [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Type 1 Diabetes (T1D) is an organ-specific autoimmune disease in which T cells are major drivers, leading to the destruction of beta-cells and insulin deficiency.
- Closing excerpt
- These results define a new antigenic region of the insulin B:9-23 peptide and demonstrate that this sequence of the B-chain becomes dramatically more antigenic when post-translationally modified through HIP formation.
- 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 (244 words)
Type 1 Diabetes (T1D) is an organ-specific autoimmune disease in which T cells are major drivers, leading to the destruction of beta-cells and insulin deficiency. Although the B-chain of insulin is a critical target for islet-reactive CD4 T cells, the native sequence is poorly antigenic and in vivo, insulin elicits only a weak Th1 response. We previously reported that post-translational modification of proinsulin through hybrid insulin peptide (HIP) formation leads to the synthesis of potent epitopes for islet-reactive CD4 T cells, and that cathepsin D (catD), a protease present in beta-cells, can mediate the formation of HIPs through a transpeptidation process. In the present study, we defined the specificity of catD for the insulin B-chain and show a high specificity for proteolytic cleavage following the disease-critical tyrosine 16 residue. We therefore hypothesized that HIP formation occurs at this amino acid. We designed a panel of HIPs containing insB9-16 fragments linked to different secretory granule proteins and challenged splenocytes isolated from diabetic NOD mice with insB9-16 HIPs; ELISPOT analysis showed elevated inflammatory responses to several peptides. Among this panel of HIPs, we identified the 2.40HIP, a fusion peptide between insB9-16 and the C-peptide, as a potent epitope recognized by PD12-2.40, a diabetogenic CD4 T cell clone isolated from the islets of a 12-week-old NOD mouse. These results define a new antigenic region of the insulin B:9-23 peptide and demonstrate that this sequence of the B-chain becomes dramatically more antigenic when post-translationally modified through HIP formation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42591790 · DOI · PMC13462851
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 New genetic loci link adipose and insulin biology to body fat distribution [4]
- Research article Glibenclamide, metformin, and insulin for the treatment of gestational diabetes: a systematic review and meta-analysis [5]
- Research article Effects of Interrupting Prolonged Sitting with Physical Activity Breaks on Blood Glucose, Insulin and Triacylglycerol Measures: A Systematic Review and Meta-analysis [6]
- Research article Diabetes mellitus and risk of falls in older adults: a systematic review and meta-analysis [7]
- Research article Management of type 2 diabetes with the dual GIP/GLP-1 receptor agonist tirzepatide: a systematic review and meta-analysis [8]
- Research article Short-term intensive insulin therapy in type 2 diabetes mellitus: a systematic review and meta-analysis [9]
References
- Ibrahim R, Froschauer C, Broschk S, Sannino DR, Dobson AJ. Lifespan and Fecundity Impacts of Reduced Insulin Signalling Can Be Directed by Mito-Nuclear Epistasis in Drosophila. . 2026. PMID 41640114 · DOI · PMC12873451
- Kejriwal N, Bouslov D, Castle CR, Karve RS, Arkharova GA, Sargsyan A, et al.. Glucagon promotes net hepatic glycogen repletion following meal ingestion. . 2026. PMID 41774508 · DOI · PMC13135395
- Wenzlau JM, Mangold K, Nicholson K, Dang M, Hohenstein AC, Douglas KS, et al.. A novel region of the insulin B9-23 sequence is targeted by a HIP-reactive diabetogenic T cell clone. . 2026. PMID 42591790 · DOI · PMC13462851
- Shungin D, Winkler TW, Croteau-Chonka DC, Ferreira T, Locke AE, Mägi R, et al.. New genetic loci link adipose and insulin biology to body fat distribution. Nature. 2015. PMID 25673412 · DOI · PMC4338562
- Balsells M, García-Patterson A, Solà I, Roqué M, Gich I, Corcoy R. Glibenclamide, metformin, and insulin for the treatment of gestational diabetes: a systematic review and meta-analysis. BMJ. 2015. PMID 25609400 · DOI · PMC4301599
- Loh R, Stamatakis E, Folkerts D, Allgrove JE, Moir HJ. Effects of Interrupting Prolonged Sitting with Physical Activity Breaks on Blood Glucose, Insulin and Triacylglycerol Measures: A Systematic Review and Meta-analysis. Sports Med. 2020. PMID 31552570 · DOI · PMC6985064
- Yang Y, Hu X, Zhang Q, Zou R. Diabetes mellitus and risk of falls in older adults: a systematic review and meta-analysis. Age Ageing. 2016. PMID 27515679 · DOI
- Karagiannis T, Avgerinos I, Liakos A, Del Prato S, Matthews DR, Tsapas A, et al.. Management of type 2 diabetes with the dual GIP/GLP-1 receptor agonist tirzepatide: a systematic review and meta-analysis. Diabetologia. 2022. PMID 35579691 · DOI · PMC9112245
- Kramer CK, Zinman B, Retnakaran R. Short-term intensive insulin therapy in type 2 diabetes mellitus: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 2013. PMID 24622264 · 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.