ReviewUpsala journal of medical sciences2016
Glucagon secretion from pancreatic α-cells.
Review in Upsala journal of medical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 64 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 110 citations in OpenAlex.
- Temporal Patterns of Glucagon and Its Relationships with Glucose and Insulin following Ingestion of Different Classes of Macronutrients.Nutrients · 2022Trial
- Increased ADORA1 expression in pancreatic islets coincides with insulin secretory defects in human type 2 diabetes.The Journal of biological chemistry · 2026Article
- β-Cell Obligation in α-Cell Glucagon Response to Low Glucose.Research square · 2026Article
- Proinflammatory cytokine-induced alpha cell impairment in human islet microtissues is partially restored by dual incretin receptor agonism.Diabetologia · 2025Article
- Glucagon in metabolic disease: a mini-review of emerging multi-organ roles beyond glycemic control.Frontiers in endocrinology · 2025Review
- Regulatory Role of Fatty Acid Metabolism on Glucose-Induced Changes in Insulin and Glucagon Secretion by Pancreatic Islet Cells.International journal of molecular sciences · 2024Review
- An extended minimal model of OGTT: estimation of α- and β-cell dysfunction, insulin resistance, and the incretin effect.American journal of physiology. Endocrinology and metabolism · 2024Article
- Kinetic Modeling of Hepatic Metabolism and Simulation of Treatment Effects.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Peroxisomes during postnatal development of mouse endocrine and exocrine pancreas display cell-type- and stage-specific protein composition.Cell and tissue research · 2023Article
- Dysglycemia Shapes Visceral Adipose Tissue's Response to GIP, GLP-1 and Glucagon in Individuals with Obesity.Metabolites · 2023Article
- Pharmacologic inhibition of somatostatin receptor 2 to restore glucagon counterregulation in diabetes.Frontiers in pharmacology · 2023Review
- Article
- Importance of multiple endocrine cell types in islet organoids for type 1 diabetes treatment.Translational research : the journal of laboratory and clinical medicine · 2022Review
- INGAP-Peptide Variants as a Novel Therapy for Type 1 Diabetes: Effect on Human Islet Insulin Secretion and Gene Expression.Pharmaceutics · 2022Article
- 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
- Acetyl-CoA-carboxylase 1 (ACC1) plays a critical role in glucagon secretion.Communications biology · 2022Article
- Heterogenous impairment of α cell function in type 2 diabetes is linked to cell maturation state.Cell metabolism · 2022Article
- Circadian rhythms and pancreas physiology: A review.Frontiers in endocrinology · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedErratum.2016
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Type 2 diabetes involves a ménage à trois of impaired glucose regulation of pancreatic hormone release: in addition to impaired glucose-induced insulin secretion, the release of the hyperglycaemic hormone glucagon becomes dysregulated; these last-mentioned defects exacerbate the metabolic consequences of hypoinsulinaemia and are compounded further by hypersecretion of somatostatin (which inhibits both insulin and glucagon secretion). Glucagon secretion has been proposed to be regulated by either intrinsic or paracrine mechanisms, but their relative significance and the conditions under which they operate are debated. Importantly, the paracrine and intrinsic modes of regulation are not mutually exclusive; they could operate in parallel to control glucagon secretion. Here we have applied mathematical modelling of α-cell electrical activity as a novel means of dissecting the processes that underlie metabolic regulation of glucagon secretion. Our analyses indicate that basal hypersecretion of somatostatin and/or increased activity of somatostatin receptors may explain the loss of adequate counter-regulation under hypoglycaemic conditions, as well as the physiologically inappropriate stimulation of glucagon secretion during hyperglycaemia seen in diabetic patients. We therefore advocate studying the interaction of the paracrine and intrinsic mechanisms; unifying these processes may give a more complete picture of the regulation of glucagon secretion from α-cells than studying the individual parts.
Indexed as
Identifiers
What OpenQuestion holds
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.