ArticleEMBO molecular medicine2012
Block of Kv1.7 potassium currents increases glucose-stimulated insulin secretion.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Glucose-lowering effect of berberine on type 2 diabetes: A systematic review and meta-analysis.Frontiers in pharmacology · 2022Pooled it
- Berberine is an insulin secretagogue targeting the KCNH6 potassium channel.Nature communications · 2021Trial
- Conkazal-M1 from the MKAVA family of conotoxins: A dual-function protease inhibitor and neuroactive peptide.Protein science : a publication of the Protein Society · 2026Article
- Development and validation of an interpretable machine learning model for predicting in-hospital hypoglycemia in adults with type 1 diabetes mellitus: a multicenter retrospective study.Frontiers in endocrinology · 2026Article
- Voltage-gated potassium channels as important modulators of glucose-stimulated insulin secretion in pancreatic β-cells: insights from rodent and human studies.Frontiers in endocrinology · 2026Review
- Conkazal-M1 from the MKAVA family of conotoxins - a dual-function protease inhibitor and neuroactive peptide.bioRxiv : the preprint server for biology · 2025Article
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- Peptide Toxins from MarineToxins · 2024Review
- Voltage-Gated KMarine drugs · 2024Review
- Venom-derived peptides for breaking through the glass ceiling of drug development.Frontiers in chemistry · 2024Review
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- µ-Theraphotoxin Pn3a inhibition of CaeLife · 2022Article
- Pathophysiological Responses to Conotoxin Modulation of Voltage-Gated Ion Currents.Marine drugs · 2022Review
- Absolute Structure Determination and Kv1.5 Ion Channel Inhibition Activities of New Debromoaplysiatoxin Analogues.Marine drugs · 2021Article
- Melatonin ameliorates hypertension in hypertensive pregnant mice and suppresses the hypertension-induced decrease in CaHypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Redox Homeostasis in Pancreatic β-Cells: From Development to Failure.Antioxidants (Basel, Switzerland) · 2021Review
- The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021Review
- Therapeutic Potential of Peptides Derived from Animal Venoms: Current Views and Emerging Drugs for Diabetes.Clinical medicine insights. Endocrinology and diabetes · 2021Review
- Marine Toxins Targeting Kv1 Channels: Pharmacological Tools and Therapeutic Scaffolds.Marine drugs · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Glucose-stimulated insulin secretion (GSIS) relies on repetitive, electrical spiking activity of the beta cell membrane. Cyclic activation of voltage-gated potassium channels (K(v) ) generates an outward, 'delayed rectifier' potassium current, which drives the repolarizing phase of each spike and modulates insulin release. Although several K(v) channels are expressed in pancreatic islets, their individual contributions to GSIS remain incompletely understood. We take advantage of a naturally occurring cone-snail peptide toxin, Conkunitzin-S1 (Conk-S1), which selectively blocks K(v) 1.7 channels to provide an intrinsically limited, finely graded control of total beta cell delayed rectifier current and hence of GSIS. Conk-S1 increases GSIS in isolated rat islets, likely by reducing K(v) 1.7-mediated delayed rectifier currents in beta cells, which yields increases in action potential firing and cytoplasmic free calcium. In rats, Conk-S1 increases glucose-dependent insulin secretion without decreasing basal glucose. Thus, we conclude that K(v) 1.7 contributes to the membrane-repolarizing current of beta cells during GSIS and that block of this specific component of beta cell K(v) current offers a potential strategy for enhancing GSIS with minimal risk of hypoglycaemia during metabolic disorders such as Type 2 diabetes.
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What Socratic 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 Socratic graph.