ArticleThe Journal of physiology2002
Glucose-dependent regulation of rhythmic action potential firing in pancreatic beta-cells by K(ATP)-channel modulation.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed.
- Intermittent hypoxia training in prediabetes patients: Beneficial effects on glucose homeostasis, hypoxia tolerance and gene expression.Experimental biology and medicine (Maywood, N.J.) · 2017Trial
- Loss of tetraspanin-7 expression reduces pancreatic β-cell exocytosis CaDiabetic medicine : a journal of the British Diabetic Association · 2022Article
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- NMDA receptor inhibition increases, synchronizes, and stabilizes the collective pancreatic beta cell activity: Insights through multilayer network analysis.PLoS computational biology · 2021Article
- 'Resistance is futile?' - paradoxical inhibitory effects of KThe Journal of physiology · 2020Review
- Microelectrode Array based Functional Testing of Pancreatic Islet Cells.Micromachines · 2020Article
- Possible New Strategies for the Treatment of Congenital Hyperinsulinism.Frontiers in endocrinology · 2020Article
- Glucose-mediated inhibition of calcium-activated potassium channels limits α-cell calcium influx and glucagon secretion.American journal of physiology. Endocrinology and metabolism · 2019Article
- Cytokine-mediated changes in KScientific reports · 2018Article
- Calcium dynamics control K-ATP channel-mediated bursting in substantia nigra dopamine neurons: a combined experimental and modeling study.Journal of neurophysiology · 2018Article
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Review
- Improving the physiological realism of experimental models.Interface focus · 2016Review
- Article
- Modeling K,ATP--dependent excitability in pancreatic islets.Biophysical journal · 2014Article
- Na+ current properties in islet α- and β-cells reflect cell-specific Scn3a and Scn9a expression.The Journal of physiology · 2014Article
- MicroRNA-7a regulates pancreatic β cell function.The Journal of clinical investigation · 2014Article
- K(ATP) channels and islet hormone secretion: new insights and controversies.Nature reviews. Endocrinology · 2013Review
- Ionic mechanisms and Ca2+ dynamics underlying the glucose response of pancreatic β cells: a simulation study.The Journal of general physiology · 2011Article
- Bursting and calcium oscillations in pancreatic beta-cells: specific pacemakers for specific mechanisms.American journal of physiology. Endocrinology and metabolism · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of a K(+) current activating during oscillatory electrical activity (I(K,slow)) in an insulin-releasing beta-cell was studied by applying the perforated patch whole-cell technique to intact mouse pancreatic islets. The resting whole-cell conductance in the presence of 10 mM glucose amounted to 1.3 nS, which rose by 50 % during a series of 26 simulated action potentials. Application of the K(ATP)-channel blocker tolbutamide produced uninterrupted action potential firing and reduced I(K,slow) by approximately 50 %. Increasing glucose from 15 to 30 mM, which likewise converted oscillatory electrical activity into continuous action potential firing, reduced I(K,slow) by approximately 30 % whilst not affecting the resting conductance. Action potential firing may culminate in opening of K(ATP) channels by activation of ATP-dependent Ca(2+) pumping as suggested by the observation that the sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin (4 microM) inhibited I(K,slow) by 25 % and abolished bursting electrical activity. We conclude that oscillatory glucose-induced electrical activity in the beta-cell involves the opening of K(ATP)-channel activity and that these channels, in addition to constituting the glucose-regulated K(+) conductance, also play a role in the graded response to supra-threshold glucose concentrations.
Indexed as
Identifiers
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.