ReviewNature reviews. Endocrinology2013
K(ATP) channels and islet hormone secretion: new insights and controversies.
Review in Nature reviews. Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.
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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.
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Who cites it
147 citing papers in PubMed, 260 citations in OpenAlex.
- Postnatal refinement of CaChannels (Austin, Tex.) · 2026Article
- Pancreatic nerves across species: Anatomical and functional disparities and their metabolic ramifications.World journal of methodology · 2026Review
- Hypoglycemic conditions enhance neonatal β-cell glucose responsiveness via AMPK/mTOR-increased KATP channel density.Endocrinology · 2026Article
- Exercise preserves β-cell function in type 2 diabetes by reshaping intra-islet macrophage-β-cell crosstalk.Life metabolism · 2026Article
- A rare case of gliclazide-induced symptomatic bradycardia in type 2 diabetes mellitus.JCEM case reports · 2026Article
- Gene expression profiles associated with stimulus-responsive insulin secretion in insulinoma.Endocrine connections · 2026Article
- Presenilin-1 controls glycolysis and identity of pancreatic beta cells.Communications biology · 2026Article
- Organelle-specific crosstalk between calcium and redox signaling in pancreatic β-cells in physiology and type 2 diabetes.Frontiers in network physiology · 2026Review
- Modulation of gene expression by traditional Asian antidiabetic nutraceuticals: A review of potential effects.Asia Pacific journal of clinical nutrition · 2025Review
- Dolutegravir-associated hyperglycemia: a narrative review.AIDS research and therapy · 2025Review
- LRRC8 channel complexes counterbalance KATP channels to mediate swell-secretion coupling in mouse pancreatic β cells.JCI insight · 2025Article
- Osmosensor TMEM63B facilitates insulin secretion in pancreatic β-cells.Science China. Life sciences · 2025Article
- KATP Channels as Target for Remodeling Connectivity in Type 2 Diabetes.Function (Oxford, England) · 2025Article
- Systemic Glucose Homeostasis Requires Pancreatic but Not Neuronal ATP-sensitive Potassium Channels.Function (Oxford, England) · 2025Article
- Article
- Unraveling the Ties: Type 2 Diabetes and Parkinson's Disease - A Nano-Based Targeted Drug Delivery Approach.Current diabetes reviews · 2025Review
- Brain-Body Communication in Glucose Metabolism.Advances in experimental medicine and biology · 2025Review
- Glucokinase activators and imeglimin: new weaponry in the armamentarium against type 2 diabetes.BMJ open diabetes research & care · 2024Review
- Extracellular matrix stiffness mediates insulin secretion in pancreatic islets via mechanosensitive Piezo1 channel regulated CaMatrix biology plus · 2024Article
- Molecular mechanism responsible for sex differences in electrical activity of mouse pancreatic β cells.JCI insight · 2024Article
87 more citing papers are in PubMed but not listed here.
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
ATP-sensitive potassium channels (K(ATP) channels) link cell metabolism to electrical activity by controlling the cell membrane potential. They participate in many physiological processes but have a particularly important role in systemic glucose homeostasis by regulating hormone secretion from pancreatic islet cells. Glucose-induced closure of K(ATP) channels is crucial for insulin secretion. Emerging data suggest that K(ATP) channels also play a key part in glucagon secretion, although precisely how they do so remains controversial. This Review highlights the role of K(ATP) channels in insulin and glucagon secretion. We discuss how K(ATP) channels might contribute not only to the initiation of insulin release but also to the graded stimulation of insulin secretion that occurs with increasing glucose concentrations. The various hypotheses concerning the role of K(ATP) channels in glucagon release are also reviewed. Furthermore, we illustrate how mutations in K(ATP) channel genes can cause hyposecretion or hypersecretion of insulin, as in neonatal diabetes mellitus and congenital hyperinsulinism, and how defective metabolic regulation of the channel may underlie the hypoinsulinaemia and the hyperglucagonaemia that characterize type 2 diabetes mellitus. Finally, we outline how sulphonylureas, which inhibit K(ATP) channels, stimulate insulin secretion in patients with neonatal diabetes mellitus or type 2 diabetes mellitus, and suggest their potential use to target the glucagon secretory defects found in diabetes mellitus.
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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.