ArticleNature communications2020
Paracrine control of α-cell glucagon exocytosis is compromised in human type-2 diabetes.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 99 citations in OpenAlex.
- Aging Affects Pancreatic α-Cell Function and Promotes Hyperglucagonemia: Implications in Age-Associated Diabetes.Aging cell · 2026Article
- Somatostatin receptors shape insulin and glucagon output within the pancreatic islet in mice through direct and paracrine effects.Diabetologia · 2026Article
- Stathmin-2 mediates paracrine hormone regulation of glucagon through lysosomal trafficking in αTC1-6 cells.The Journal of physiology · 2026Article
- Intra-Islet Paracrine Regulation of Glucagon Secretion During Hypoglycemia, Euglycemia, and Hyperglycemia.Annals of the New York Academy of Sciences · 2026Review
- Peripheral GABA Signaling in Metabolic Adaptation and Maladaptation.International journal of molecular sciences · 2026Review
- Temporal single-cell transcriptional dynamics of murine pancreatic islet remodeling during hyperglycaemia progression.Molecular metabolism · 2026Article
- Ghrelin and relamorelin counteract hypoglycemia in mice engrafted with congenital hyperinsulinism stem cell-derived islets.Stem cells translational medicine · 2026Article
- From beta-cell failure to islet dysfunction: the emerging role of the alpha cell.BMJ open diabetes research & care · 2026Article
- Transient fetal hyperglycemia reprograms adipogenesis, lipogenesis, and insulin signaling in zebrafish.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Heterogeneous endocrine cell composition defines human islet functional phenotypes.Nature communications · 2026Article
- Advances in Internal Organogenesis: Differentiation and Morphogenesis of Human Ventral Cavity Organs.Stem cell reviews and reports · 2026Review
- Somatostatin Receptors Shape Insulin and Glucagon Output within the Pancreatic Islet through Direct and Paracrine Effects.bioRxiv : the preprint server for biology · 2025Article
- Genome-wide CRISPR Screen Identifies Sec31A as a Key Regulator of Alpha Cell Survival.Nature communications · 2025Article
- Heterogeneous endocrine cell composition defines human islet functional phenotypes.bioRxiv : the preprint server for biology · 2025Article
- 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
- Review Article: GLP-1 Receptor Agonists and Glucagon/GIP/GLP-1 Receptor Dual or Triple Agonists-Mechanism of Action and Emerging Therapeutic Landscape in MASLD.Alimentary pharmacology & therapeutics · 2025Review
- Dehydration-induced AVP stimulates glucagon release and ketogenesis.American journal of physiology. Endocrinology and metabolism · 2025Article
- Blockade of glucagon receptor induces α-cell hypersecretion by hyperaminoacidemia in mice.Nature communications · 2025Article
- Real-time detection of somatostatin release from single islets reveals hypersecretion in type 2 diabetes.Acta physiologica (Oxford, England) · 2025Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucagon is released from pancreatic α-cells to activate pathways that raise blood glucose. Its secretion is regulated by α-cell-intrinsic glucose sensing and paracrine control through insulin and somatostatin. To understand the inadequately high glucagon levels that contribute to hyperglycemia in type-2 diabetes (T2D), we analyzed granule behavior, exocytosis and membrane excitability in α-cells of 68 non-diabetic and 21 T2D human donors. We report that exocytosis is moderately reduced in α-cells of T2D donors, without changes in voltage-dependent ion currents or granule trafficking. Dispersed α-cells have a non-physiological V-shaped dose response to glucose, with maximal exocytosis at hyperglycemia. Within intact islets, hyperglycemia instead inhibits α-cell exocytosis, but not in T2D or when paracrine inhibition by insulin or somatostatin is blocked. Surface expression of somatostatin-receptor-2 is reduced in T2D, suggesting a mechanism for the observed somatostatin resistance. Thus, elevated glucagon in human T2D may reflect α-cell insensitivity to paracrine inhibition at hyperglycemia.
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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 Socratic graph.