ArticleCell metabolism2013
Role of KATP channels in glucose-regulated glucagon secretion and impaired counterregulation in type 2 diabetes.
Article in Cell metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05616273 (Stimulated Glucagon as a Biomarker of Hypoglycemic Risk in Type 1 Diabetes), which is not on this map. Cited by 141 papers.
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.
Stimulated Glucagon as a Biomarker of Hypoglycemic Risk in Type 1 Diabetes
Who cites it
141 citing papers in PubMed, 223 citations in OpenAlex.
- Trial
- Temporal Patterns of Glucagon and Its Relationships with Glucose and Insulin following Ingestion of Different Classes of Macronutrients.Nutrients · 2022Trial
- Proteomic analysis of pancreatic endocrine cells by mechanistic single-cell isolation identifies membrane pathways.Experimental & molecular medicine · 2026Article
- Intra-Islet Paracrine Regulation of Glucagon Secretion During Hypoglycemia, Euglycemia, and Hyperglycemia.Annals of the New York Academy of Sciences · 2026Review
- Highly selective SGLT2 inhibitors suppress glucose uptake in alpha-TC1 cells, while glucagon secretion is not affected.Hormones (Athens, Greece) · 2026Article
- Pancreatic α-cells are functionally heterogeneous and sex-dependently regulated by neighboring endocrine cells.Communications biology · 2026Article
- Real-time autonomic responses to insulin-induced hypoglycaemia in volunteers with type I diabetes compared to controls.IBRO neuroscience reports · 2026Article
- β-Cell Obligation in α-Cell Glucagon Response to Low Glucose.Research square · 2026Article
- Paracrine inhibition via G protein inwardly rectifying potassium channels regulates glucagon secretion from human pancreatic alpha cells.Cell reports · 2026Article
- Article
- Loss of Beta-Cell Identity and Function as a Mechanism of Secondary Failure of Sulfonylurea Therapy in Diabetes.MedComm · 2026Article
- Antecedent hypoglycaemia impairs glucagon secretion by enhancing somatostatin-mediated negative feedback control.Nature metabolism · 2026Article
- Oral Treatment of Obesity by GLP-1 and Its Analogs.Pharmaceutics · 2025Review
- Review
- Imeglimin suppresses glucagon secretion and induces a loss of α cell identity.Cell reports. Medicine · 2025Article
- Reprogramming of Different Cell Lineages into Functional β-Cell Substitutes.Cellular reprogramming · 2025Review
- TMEM55A-mediated PI5P signalling regulates alpha cell actin depolymerisation and glucagon secretion.Diabetologia · 2025Article
- Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells.Stem cell reports · 2025Article
- Amino acid sensing by the α-cell mitochondrial phosphoenolpyruvate cycle regulates intracellular CabioRxiv : the preprint server for biology · 2025Article
- 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
81 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
22 authors at 5 institutions in 1 country.
Funding
Abstract
Glucagon, secreted by pancreatic islet α cells, is the principal hyperglycemic hormone. In diabetes, glucagon secretion is not suppressed at high glucose, exacerbating the consequences of insufficient insulin secretion, and is inadequate at low glucose, potentially leading to fatal hypoglycemia. The causal mechanisms remain unknown. Here we show that α cell KATP-channel activity is very low under hypoglycemic conditions and that hyperglycemia, via elevated intracellular ATP/ADP, leads to complete inhibition. This produces membrane depolarization and voltage-dependent inactivation of the Na(+) channels involved in action potential firing that, via reduced action potential height and Ca(2+) entry, suppresses glucagon secretion. Maneuvers that increase KATP channel activity, such as metabolic inhibition, mimic the glucagon secretory defects associated with diabetes. Low concentrations of the KATP channel blocker tolbutamide partially restore glucose-regulated glucagon secretion in islets from type 2 diabetic organ donors. These data suggest that impaired metabolic control of the KATP channels underlies the defective glucose regulation of glucagon secretion in type 2 diabetes.
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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.