ArticleBritish journal of pharmacology2010
Pharmacological stimulation and inhibition of insulin secretion in mouse islets lacking ATP-sensitive K+ channels.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Dopaminergic modulation of pancreatic beta-cell insulin secretion and implications for antipsychotic-induced glucose dysregulation: a systematic review and meta-analysis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Pooled it
- The contrasting effects of two antimalarial drugs on insulin secretion.Cellular and molecular life sciences : CMLS · 2025Article
- Quinine: rediscovery of an old glucose-lowering drug.Diabetologia · 2025Article
- Article
- BetaBuddy: An automated end-to-end computer vision pipeline for analysis of calcium fluorescence dynamics in β-cells.PloS one · 2024Article
- Diazoxide-Induced Hypertrichosis in a Neonate With Transient Hyperinsulinism.Clinical medicine insights. Case reports · 2023Article
- Contribution of Mitochondria to Insulin Secretion by Various Secretagogues.Antioxidants & redox signaling · 2022Review
- Celebrities in the heart, strangers in the pancreatic beta cell: Voltage-gated potassium channels KActa physiologica (Oxford, England) · 2022Review
- Decreased KATP Channel Activity Contributes to the Low Glucose Threshold for Insulin Secretion of Rat Neonatal Islets.Endocrinology · 2021Article
- The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Evidence that the multiflorine-derived substituted quinazolidine 55P0251 augments insulin secretion and lowers blood glucose via antagonism at αDiabetes, obesity & metabolism · 2020Article
- Hypoglycemia After Gastric Bypass Successfully Treated With Calcium Channel Blockers: Two Case Reports.Journal of the Endocrine Society · 2019Article
- Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9.Scientific reports · 2017Article
- Nifedipine in Congenital Hyperinsulinism - A Case Report.Journal of clinical research in pediatric endocrinology · 2015Article
- Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells.PloS one · 2015Article
- Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms.Sleep and biological rhythms · 2015Article
- The effect of adrenal medullectomy on metabolic responses to chronic intermittent hypoxia.Respiratory physiology & neurobiology · 2014Article
- A mouse model of human hyperinsulinism produced by the E1506K mutation in the sulphonylurea receptor SUR1.Diabetes · 2013Article
- Mechanisms of antihyperglycaemic action of efaroxan in mice: time for reappraisal of α2A-adrenergic antagonism in the treatment of type 2 diabetes?Diabetologia · 2012Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeATP-sensitive potassium channels (K(ATP) channels) in beta cells are a major target for insulinotropic drugs. Here, we studied the effects of selected stimulatory and inhibitory pharmacological agents in islets lacking K(ATP) channels. EXPERIMENTAL APPROACH: We compared insulin secretion (IS) and cytosolic calcium ([Ca(2+)](c)) changes in islets isolated from control mice and mice lacking sulphonylurea receptor1 (SUR1), and thus K(ATP) channels in their beta cells (Sur1KO). KEY
resultsWhile similarly increasing [Ca(2+)](c) and IS in controls, agents binding to site A (tolbutamide) or site B (meglitinide) of SUR1 were ineffective in Sur1KO islets. Of two non-selective blockers of potassium channels, quinine was inactive, whereas tetraethylammonium was more active in Sur1KO compared with control islets. Phentolamine, efaroxan and alinidine, three imidazolines binding to K(IR)6.2 (pore of K(ATP) channels), stimulated control islets, but only phentolamine retained weaker stimulatory effects on [Ca(2+)](c) and IS in Sur1KO islets. Neither K(ATP) channel opener (diazoxide, pinacidil) inhibited Sur1KO islets. Calcium channel blockers (nimodipine, verapamil) or diphenylhydantoin decreased [Ca(2+)](c) and IS in both types of islets, verapamil and diphenylhydantoin being more efficient in Sur1KO islets. Activation of alpha(2)-adrenoceptors or dopamine receptors strongly inhibited IS while partially (clonidine > dopamine) lowering [Ca(2+)](c) (control > Sur1KO islets). CONCLUSIONS AND IMPLICATIONS: Those drugs retaining effects on IS in islets lacking K(ATP) channels, also affected [Ca(2+)](c), indicating actions on other ionic channels. The greater effects of some inhibitors in Sur1KO than in control islets might be relevant to medical treatment of congenital hyperinsulinism caused by inactivating mutations of K(ATP) channels.
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.