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 (689 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
Production and release of insulin from pancreatic beta cells that primarily occurs in response to elevated blood glucose levels.
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: Secretion, Insulin.
Where it fits in the MeSH classification
- Broader topics
- Metabolism; Physiological Phenomena
Related concepts
- Pancreatic Beta Cells
- Blood Glucose
Research landscape
PubMed indexes 24,640 records tagged with the MeSH heading “Insulin Secretion” (counts retrieved 2026-10-31). 2,077 of them (8.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 12,140 records.
Reviews account for 3,097 records (12.6%) and meta-analyses for 27. Randomized controlled trials number 595 (2.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 12,140 |
| 2000-2009 | 5,240 |
| 2010-2019 | 5,183 |
| 2020 onward | 2,077 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,097 | 12.6% |
| Meta-analyses | 27 | 0.1% |
| Randomized controlled trials | 595 | 2.4% |
Method: PubMed query "Insulin Secretion"[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 |
|---|---|---|---|---|
| Pathophysiology of Type 2 Diabetes Mellitus | 2020 | Review article Design not recorded in structured metadata | 1,944 | cc by PMID 32872570 · DOI · PMC7503727 |
| Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments | 2020 | Review article Design not recorded in structured metadata | 180 | cc by PMID 32982969 · DOI · PMC7477770 |
| Insulin granule biogenesis and exocytosis | 2021 | Review article Design not recorded in structured metadata | 118 | cc by PMID 33146746 · DOI · PMC7966131 |
| Reduced peroxisomal function increases insulin secretion, promotes insulin oxidation, and impairs β cell maturity | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42378063 · DOI · PMC13463611 |
Pathophysiology of Type 2 Diabetes Mellitus [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin.
- Closing excerpt
- Additionally, because T2DM is associated with accelerated atherosclerosis development, we review here some of the molecular mechanisms that link T2DM and insulin resistance (IR) as well as cardiovascular risk as one of the most important complications in T2DM.
- 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 (205 words)
Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the synthesis and release of insulin, as well as in its detection are tightly regulated. Defects in any of the mechanisms involved in these processes can lead to a metabolic imbalance responsible for the development of the disease. This review analyzes the key aspects of T2DM, as well as the molecular mechanisms and pathways implicated in insulin metabolism leading to T2DM and insulin resistance. For that purpose, we summarize the data gathered up until now, focusing especially on insulin synthesis, insulin release, insulin sensing and on the downstream effects on individual insulin-sensitive organs. The review also covers the pathological conditions perpetuating T2DM such as nutritional factors, physical activity, gut dysbiosis and metabolic memory. Additionally, because T2DM is associated with accelerated atherosclerosis development, we review here some of the molecular mechanisms that link T2DM and insulin resistance (IR) as well as cardiovascular risk as one of the most important complications in T2DM.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32872570 · DOI · PMC7503727
Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Sarcopenic obesity and diabetes are two increasing health problems worldwide, which both share many common risk factors, such as aging, and general obesity.
- Closing excerpt
- This review consolidates and discusses the latest research in pathogenesis, diagnosis, and treatments of diabetes and sarcopenic obesity.
- 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 (138 words)
Sarcopenic obesity and diabetes are two increasing health problems worldwide, which both share many common risk factors, such as aging, and general obesity. The pathogenesis of sarcopenic obesity includes aging, physical inactivity, malnutrition, low-grade inflammation, insulin resistance, and hormonal changes. Nevertheless, there are two major reasons to cause diabetes: impaired insulin secretion and impaired insulin action. Furthermore, the individual diagnosis of obesity and sarcopenia should be combined to adequately define sarcopenic obesity. Also, the diagnosis of diabetes includes fasting plasma glucose test (FPG), 2-h oral glucose tolerance test (OGTT), glycated hemoglobin (A1C), and random plasma glucose coupled with symptoms. Healthy diet and physical activity are beneficial to both sarcopenic obesity and diabetes, but there are only recommended drugs for diabetes. This review consolidates and discusses the latest research in pathogenesis, diagnosis, and treatments of diabetes and sarcopenic obesity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32982969 · DOI · PMC7477770
Insulin granule biogenesis and exocytosis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Insulin is produced by pancreatic β-cells, and once released to the blood, the hormone stimulates glucose uptake and suppresses glucose production.
- Closing excerpt
- We also highlight the role of the β-cell in the development of type-2 diabetes and discuss how dysregulation of one or several steps in the insulin granule life cycle may contribute to disease development or 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 (177 words)
Insulin is produced by pancreatic β-cells, and once released to the blood, the hormone stimulates glucose uptake and suppresses glucose production. Defects in both the availability and action of insulin lead to elevated plasma glucose levels and are major hallmarks of type-2 diabetes. Insulin is stored in secretory granules that form at the trans-Golgi network. The granules undergo extensive modifications en route to their release sites at the plasma membrane, including changes in both protein and lipid composition of the granule membrane and lumen. In parallel, the insulin molecules also undergo extensive modifications that render the hormone biologically active. In this review, we summarize current understanding of insulin secretory granule biogenesis, maturation, transport, docking, priming and eventual fusion with the plasma membrane. We discuss how different pools of granules form and how these pools contribute to insulin secretion under different conditions. We also highlight the role of the β-cell in the development of type-2 diabetes and discuss how dysregulation of one or several steps in the insulin granule life cycle may contribute to disease development or progression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33146746 · DOI · PMC7966131
Reduced peroxisomal function increases insulin secretion, promotes insulin oxidation, and impairs β cell maturity [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Given the central role of peroxisomes in lipid metabolism and redox homeostasis, we hypothesized that peroxisomal activity is critical for sustaining β cell function and identity.
- Closing excerpt
- Based on these outcomes, we identified the peroxisome organelle as a key regulatory component of glucose homeostasis by protecting insulin from oxidative modification and degradation and by supporting maintenance of mature β cells.
- 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 (169 words)
Given the central role of peroxisomes in lipid metabolism and redox homeostasis, we hypothesized that peroxisomal activity is critical for sustaining β cell function and identity. Pex5 deletion models were employed to investigate the loss of peroxisomal function on glucose-stimulated insulin secretion (GSIS), oxidative stress, and β cell maturity markers. Peroxisome deficiency in male mice resulted in elevated GSIS. Glucose intolerance developed despite increased insulin secretion. Ion mobility mass spectrometry revealed oxidation of insulin proteins and a truncated insulin 2-derived peptide in islets from mice with a tissue-specific deficiency in peroxisomes. Peroxisome loss of function increased multiple markers of oxidative stress, including altered metabolite profiles, lipid peroxidation, and protein carbonylation. These findings revealed that increased secretion of oxidized insulin protein is insufficient to regulate whole-body glucose homeostasis. Peroxisome deficiency also reduced markers of β cell maturity. Based on these outcomes, we identified the peroxisome organelle as a key regulatory component of glucose homeostasis by protecting insulin from oxidative modification and degradation and by supporting maintenance of mature β cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42378063 · DOI · PMC13463611
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 Mechanisms controlling pancreatic islet cell function in insulin secretion [5]
- Research article Early beta cell dysfunction vs insulin hypersecretion as the primary event in the pathogenesis of dysglycaemia [6]
- Research article The dynamic plasticity of insulin production in β-cells [7]
- Research article Effects of Magnesium Deficiency on Mechanisms of Insulin Resistance in Type 2 Diabetes: Focusing on the Processes of Insulin Secretion and Signaling [8]
- Research article Inadequate β-cell mass is essential for the pathogenesis of type 2 diabetes [9]
- Research article Use of human islets to understand islet biology and diabetes: progress, challenges and suggestions [10]
References
- Galicia-Garcia U, Benito-Vicente A, Jebari S, Larrea-Sebal A, Siddiqi H, Uribe KB, et al.. Pathophysiology of Type 2 Diabetes Mellitus. . 2020. PMID 32872570 · DOI · PMC7503727
- Wang M, Tan Y, Shi Y, Wang X, Liao Z, Wei P. Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments. . 2020. PMID 32982969 · DOI · PMC7477770
- Omar-Hmeadi M, Idevall-Hagren O. Insulin granule biogenesis and exocytosis. . 2021. PMID 33146746 · DOI · PMC7966131
- Collier JJ, Cothern CR, Ducote MP, Martin TM, Linden MA, Noland RC, et al.. Reduced peroxisomal function increases insulin secretion, promotes insulin oxidation, and impairs β cell maturity. . 2026. PMID 42378063 · DOI · PMC13463611
- Campbell JE, Newgard CB. Mechanisms controlling pancreatic islet cell function in insulin secretion. Nat Rev Mol Cell Biol. 2021. PMID 33398164 · DOI · PMC8115730
- Esser N, Utzschneider KM, Kahn SE. Early beta cell dysfunction vs insulin hypersecretion as the primary event in the pathogenesis of dysglycaemia. Diabetologia. 2020. PMID 32894311 · DOI
- Boland BB, Rhodes CJ, Grimsby JS. The dynamic plasticity of insulin production in β-cells. Mol Metab. 2017. PMID 28951821 · DOI · PMC5605729
- Kostov K. Effects of Magnesium Deficiency on Mechanisms of Insulin Resistance in Type 2 Diabetes: Focusing on the Processes of Insulin Secretion and Signaling. Int J Mol Sci. 2019. PMID 30889804 · DOI · PMC6470576
- Weir GC, Gaglia J, Bonner-Weir S. Inadequate β-cell mass is essential for the pathogenesis of type 2 diabetes. Lancet Diabetes Endocrinol. 2020. PMID 32006519 · DOI · PMC7098467
- Hart NJ, Powers AC. Use of human islets to understand islet biology and diabetes: progress, challenges and suggestions. Diabetologia. 2019. PMID 30547228 · DOI · PMC6325002
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.