ArticleThe Journal of physiology2000
Regulation of glucagon release in mouse -cells by KATP channels and inactivation of TTX-sensitive Na+ channels.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
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Who cites it
108 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.
- The relationship between glucose and the liver-alpha cell axis - A systematic review.Frontiers in endocrinology · 2022Pooled it
- Paracrine inhibition via G protein inwardly rectifying potassium channels regulates glucagon secretion from human pancreatic alpha cells.Cell reports · 2026Article
- Loss of Beta-Cell Identity and Function as a Mechanism of Secondary Failure of Sulfonylurea Therapy in Diabetes.MedComm · 2026Article
- Hyperglucagonemia and glucagon hypersecretion in early type 2 diabetes result from multifaceted dysregulation of pancreatic mouse α-cells.Pflugers Archiv : European journal of physiology · 2025Article
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- Wnt signaling regulates ion channel expression to promote smooth muscle and cartilage formation in developing mouse trachea.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Wnt signaling regulates ion channel expression to promote smooth muscle and cartilage formation in developing mouse trachea.bioRxiv : the preprint server for biology · 2023Article
- α-cell electrophysiology and the regulation of glucagon secretion.The Journal of endocrinology · 2023Review
- Metabolic Messengers: glucagon.Nature metabolism · 2023Review
- α Cell dysfunction in islets from nondiabetic, glutamic acid decarboxylase autoantibody-positive individuals.The Journal of clinical investigation · 2022Article
- Beta-cell specific Insr deletion promotes insulin hypersecretion and improves glucose tolerance prior to global insulin resistance.Nature communications · 2022Article
- Heterogenous impairment of α cell function in type 2 diabetes is linked to cell maturation state.Cell metabolism · 2022Article
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Intercellular Communication in the Islet of Langerhans in Health and Disease.Comprehensive Physiology · 2021Article
- The Glucagon-Like Adipokinetic Hormone inFrontiers in physiology · 2021Review
- Lactate activation of α-cell KMolecular metabolism · 2020Article
- CaChannels (Austin, Tex.) · 2020Review
- Cellular and systemic mechanisms for glucose sensing and homeostasis.Pflugers Archiv : European journal of physiology · 2020Review
- Paracrine control of α-cell glucagon exocytosis is compromised in human type-2 diabetes.Nature communications · 2020Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The perforated patch whole-cell configuration of the patch-clamp technique was applied to superficial glucagon-secreting alpha-cells in intact mouse pancreatic islets. alpha-cells were distinguished from the beta- and delta-cells by the presence of a large TTX-blockable Na+ current, a TEA-resistant transient K+ current sensitive to 4-AP (A-current) and the presence of two kinetically separable Ca2+ current components corresponding to low- (T-type) and high-threshold (L-type) Ca2+ channels. The T-type Ca2+, Na+ and A-currents were subject to steady-state voltage-dependent inactivation, which was half-maximal at -45, -47 and -68 mV, respectively. Pancreatic alpha-cells were equipped with tolbutamide-sensitive, ATP-regulated K+ (KATP) channels. Addition of tolbutamide (0.1 mM) evoked a brief period of electrical activity followed by a depolarisation to a plateau of -30 mV with no regenerative electrical activity. Glucagon secretion in the absence of glucose was strongly inhibited by TTX, nifedipine and tolbutamide. When diazoxide was added in the presence of 10 mM glucose, concentrations up to 2 microM stimulated glucagon secretion to the same extent as removal of glucose. We conclude that electrical activity and secretion in the alpha-cells is dependent on the generation of Na+-dependent action potentials. Glucagon secretion depends on low activity of KATP channels to keep the membrane potential sufficiently negative to prevent voltage-dependent inactivation of voltage-gated membrane currents. Glucose may inhibit glucagon release by depolarising the alpha-cell with resultant inactivation of the ion channels participating in action potential generation.
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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.