ArticleDiabetes2013
Tolbutamide controls glucagon release from mouse islets differently than glucose: involvement of K(ATP) channels from both α-cells and δ-cells.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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
47 citing papers in PubMed, 89 citations in OpenAlex.
- Temporal Patterns of Glucagon and Its Relationships with Glucose and Insulin following Ingestion of Different Classes of Macronutrients.Nutrients · 2022Trial
- Effect of exenatide, sitagliptin, or glimepiride on β-cell secretory capacity in early type 2 diabetes.Diabetes care · 2014Trial
- Loss of Beta-Cell Identity and Function as a Mechanism of Secondary Failure of Sulfonylurea Therapy in Diabetes.MedComm · 2026Article
- Real-time detection of somatostatin release from single islets reveals hypersecretion in type 2 diabetes.Acta physiologica (Oxford, England) · 2025Article
- The role of mu-opioid receptors in pancreatic islet α-cells.Journal of molecular endocrinology · 2025Article
- Leucine Suppresses α-Cell cAMP and Glucagon Secretion via a Combination of Cell-Intrinsic and Islet Paracrine Signaling.Diabetes · 2024Article
- The role of mu-opioid receptors in pancreatic islet alpha cells.bioRxiv : the preprint server for biology · 2024Article
- α-cell electrophysiology and the regulation of glucagon secretion.The Journal of endocrinology · 2023Review
- Glucose inhibits glucagon secretion by decreasing [CaMolecular metabolism · 2022Article
- α Cell dysfunction in islets from nondiabetic, glutamic acid decarboxylase autoantibody-positive individuals.The Journal of clinical investigation · 2022Article
- Article
- Lactate activation of α-cell KMolecular metabolism · 2020Article
- 'Resistance is futile?' - paradoxical inhibitory effects of KThe Journal of physiology · 2020Review
- Reduced somatostatin signalling leads to hypersecretion of glucagon in mice fed a high-fat diet.Molecular metabolism · 2020Article
- γ-Hydroxybutyrate does not mediate glucose inhibition of glucagon secretion.The Journal of biological chemistry · 2020Article
- Modelling of dysregulated glucagon secretion in type 2 diabetes by considering mitochondrial alterations in pancreatic α-cells.Royal Society open science · 2020Article
- Integrating the inputs that shape pancreatic islet hormone release.Nature metabolism · 2019Review
- Abnormal regulation of glucagon secretion by human islet alpha cells in the absence of beta cells.EBioMedicine · 2019Article
- Obesity dysregulates fasting-induced changes in glucagon secretion.The Journal of endocrinology · 2019Article
- Glucose stimulates somatostatin secretion in pancreatic δ-cells by cAMP-dependent intracellular CaThe Journal of general physiology · 2019Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We evaluated the role of ATP-sensitive K⁺ (K(ATP)) channels, somatostatin, and Zn²⁺ in the control of glucagon secretion from mouse islets. Switching from 1 to 7 mmol/L glucose inhibited glucagon release. Diazoxide did not reverse the glucagonostatic effect of glucose. Tolbutamide decreased glucagon secretion at 1 mmol/L glucose (G1) but stimulated it at 7 mmol/L glucose (G7). The reduced glucagon secretion produced by high concentrations of tolbutamide or diazoxide, or disruption of K(ATP) channels (Sur1(-/-) mice) at G1 could be inhibited further by G7. Removal of the somatostatin paracrine influence (Sst(-/-) mice or pretreatement with pertussis toxin) strongly increased glucagon release, did not prevent the glucagonostatic effect of G7, and unmasked a marked glucagonotropic effect of tolbutamide. Glucose inhibited glucagon release in the absence of functional K(ATP) channels and somatostatin signaling. Knockout of the Zn²⁺ transporter ZnT8 (ZnT8(-/-) mice) did not prevent the glucagonostatic effect of glucose. In conclusion, glucose can inhibit glucagon release independently of Zn²⁺, K(ATP) channels, and somatostatin. Closure of K(ATP) channels controls glucagon secretion by two mechanisms, a direct stimulation of α-cells and an indirect inhibition via somatostatin released from δ-cells. The net effect on glucagon release results from a balance between both effects.
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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.