ArticleDiabetes2010
ATP-sensitive K+ channel mediates the zinc switch-off signal for glucagon response during glucose deprivation.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 61 citations in OpenAlex.
- Regulation of glucagon secretion in normal and diabetic human islets by γ-hydroxybutyrate and glycine.The Journal of biological chemistry · 2013Trial
- Zinc Homeostasis and the Risk of Type 2 Diabetes: Complex Role of ZnT8 in Insulin and Glucagon Secretion.Current nutrition reports · 2026Review
- α-cell electrophysiology and the regulation of glucagon secretion.The Journal of endocrinology · 2023Review
- Loss of Znt8 function in diabetes mellitus: risk or benefit?Molecular and cellular biochemistry · 2021Review
- Intercellular Communication in the Islet of Langerhans in Health and Disease.Comprehensive Physiology · 2021Article
- Carvedilol prevents impairment of the counterregulatory response in recurrently hypoglycaemic diabetic rats.Endocrinology, diabetes & metabolism · 2021Article
- αFrontiers in cell and developmental biology · 2020Article
- Zinc and its regulators in pancreas.Inflammopharmacology · 2019Review
- Decrease of γ-aminobutyric acid and zinc ions in the islet periportal circulation stimulates glucagon secretion during hypoglycemia.Experimental and therapeutic medicine · 2018Article
- Zinc status is associated with inflammation, oxidative stress, lipid, and glucose metabolism.The journal of physiological sciences : JPS · 2018Review
- Silymarin Activates c-AMP Phosphodiesterase and Stimulates Insulin Secretion in a Glucose-Dependent Manner in HIT-T15 Cells.Antioxidants (Basel, Switzerland) · 2016Article
- Glucose control of glucagon secretion-'There's a brand-new gimmick every year'.Upsala journal of medical sciences · 2016Review
- Zinc and diabetes mellitus: understanding molecular mechanisms and clinical implications.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2015Review
- Zinc and insulin in pancreatic beta-cells.Endocrine · 2014Review
- Article
- Influence of VMH fuel sensing on hypoglycemic responses.Trends in endocrinology and metabolism: TEM · 2013Review
- The diabetes-susceptible gene SLC30A8/ZnT8 regulates hepatic insulin clearance.The Journal of clinical investigation · 2013Article
- Extracellular zinc ion regulates transient receptor potential melastatin 5 (TRPM5) channel activation through its interaction with a pore loop domain.The Journal of biological chemistry · 2013Article
- Early loss of the glucagon response to hypoglycemia in adolescents with type 1 diabetes.Diabetes care · 2012Article
- Glucose decouples intracellular Ca2+ activity from glucagon secretion in mouse pancreatic islet alpha-cells.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe intraislet insulin hypothesis proposes that glucagon secretion during hypoglycemia is triggered by a decrease in intraislet insulin secretion. A more recent hypothesis based on in vivo data from hypoglycemic rats is that it is the decrease in zinc cosecreted with insulin from beta-cells, rather than the decrease in insulin itself, that signals glucagon secretion from alpha-cells during hypoglycemia. These studies were designed to determine whether closure of the alpha-cell ATP-sensitive K(+) channel (K(ATP) channel) is the mechanism through which the zinc switch-off signal triggers glucagon secretion during glucose deprivation. RESEARCH DESIGN AND
methodsAll studies were performed using perifused isolated islets.
resultsIn control experiments, the expected glucagon response to an endogenous insulin switch-off signal during glucose deprivation was observed in wild-type mouse islets. In experiments with streptozotocin-treated wild-type islets, a glucagon response to an exogenous zinc switch-off signal was observed during glucose deprivation. However, this glucagon response to the zinc switch-off signal during glucose deprivation was not seen in the presence of nifedipine, diazoxide, or tolbutamide or if K(ATP) channel knockout mouse islets were used. All islets had intact glucagon responses to epinephrine.
conclusionsThese data demonstrate that closure of K(ATP) channels and consequent opening of calcium channels is the mechanism through which the zinc switch-off signal triggers glucagon secretion during glucose deprivation.
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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.