ReviewDiabetes, obesity & metabolism2012
The diabetic β-cell: hyperstimulated vs. hyperexcited.
Review in Diabetes, obesity & metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- The Downregulation of Type 1 Diabetes Susceptibility Gene PGM1 Induces Metabolic Imbalance and Stress in Pancreatic β-Cells.Diabetes · 2026Article
- Upregulation of hepatic flavin-containing monooxygenase 3 by increased corticosterone via glucocorticoid receptor contributes to gestational diabetes mellitus.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- The WCIRDC 2023: Concepts of insulin resistance.Journal of diabetes · 2024Article
- The nuclear localization sequence and C-terminus of parathyroid hormone-related protein regulate normal pancreatic islet development and function.General and comparative endocrinology · 2023Article
- Comparative Attenuating Impact of Camel Milk and Insulin in Streptozotocin-Induced Diabetic Albino Rats.ACS omega · 2023Article
- Glucokinase Inhibition: A Novel Treatment for Diabetes?Diabetes · 2023Review
- Evaluation of Major Constituents of Medicinally Important Plants for Anti-Inflammatory, Antidiabetic and AGEs Inhibiting Properties: In Vitro and Simulatory Evidence.Molecules (Basel, Switzerland) · 2022Article
- Genetic Reduction of Glucose Metabolism Preserves Functional β-Cell Mass in KATP-Induced Neonatal Diabetes.Diabetes · 2022Article
- Persistent organic pollutants and β-cell toxicity: a comprehensive review.American journal of physiology. Endocrinology and metabolism · 2022Review
- Isolation and Proteomics of the Insulin Secretory Granule.Metabolites · 2021Review
- Type 2 diabetes: one disease, many pathways.American journal of physiology. Endocrinology and metabolism · 2020Article
- The role of membrane excitability in pancreatic β-cell glucotoxicity.Scientific reports · 2019Article
- A novel high-affinity inhibitor against the human ATP-sensitive Kir6.2 channel.The Journal of general physiology · 2018Article
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Control of Kir channel gating by cytoplasmic domain interface interactions.The Journal of general physiology · 2017Article
- Islet Hypersensitivity to Glucose Is Associated With Disrupted Oscillations and Increased Impact of Proinflammatory Cytokines in Islets From Diabetes-Prone Male Mice.Endocrinology · 2016Article
- Potentiation of Calcium Influx and Insulin Secretion in Pancreatic Beta Cell by the Specific TREK-1 Blocker Spadin.Journal of diabetes research · 2016Article
- Article
- Impact of streptozotocin on altering normal glucose homeostasis during insulin testing in diabetic rats compared to normoglycemic rats.Drug design, development and therapy · 2015Article
- Ionic mechanisms in pancreatic β cell signaling.Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hyperglycaemia has multiple effects on β-cells, some clearly prosecretory, including hyperplasia and elevated insulin content, but eventually, a 'glucotoxic' effect which leads to pancreatic β-cell dysfunction, reduced β-cell mass and insulin deficiency, is an important part of diabetes pathophysiology. Myriad underlying cellular and molecular processes could lead to such dysfunction. High glucose will stimulate glycolysis and oxidative phosphorylation, which will in turn increase β-cell membrane excitability through K(ATP) channel closure. Chronic hyperexcitability will then lead to persistently elevated [Ca(2+)](i), a key trigger to insulin secretion. Thus, at least a part of the consequence of 'hyperstimulation' by glucose has been suggested to be a result of 'hyperexcitability' and chronically elevated [Ca(2+)](i). This link is lost when the [glucose], K(ATP) -channel activity link is broken, either pharmacologically or genetically. In isolated islets, such studies reveal that hyperexcitability causes a largely reversible chronic loss of insulin content, but in vivo chronic hyperexcitability per se does not lead to β-cell death or loss of insulin content. On the other hand, chronic inexcitability in vivo leads to systemic diabetes and consequential β-cell death, even while [Ca(2+)](i) remains low.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.