ArticlePloS one2009
Glucagon-like peptide-1 induced signaling and insulin secretion do not drive fuel and energy metabolism in primary rodent pancreatic beta-cells.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 64 citations in OpenAlex.
- Metabolic state determines the brain and direct islet effects of liraglutide on enhanced insulin secretion.Diabetologia · 2026Article
- The effects of liraglutide on expressions of insulin secretion and beta cell survive associated GPCR genes in pancreatic beta cells.Turkish journal of medical sciences · 2025Article
- Pancreatic beta-cell mass and function and therapeutic implications of using antidiabetic medications in type 2 diabetes.Journal of diabetes investigation · 2024Review
- Light-Mediated Enhancement of Glucose-Stimulated Insulin Release of Optogenetically Engineered Human Pancreatic Beta-Cells.ACS synthetic biology · 2024Article
- A Comprehensive Review on GLP-1 Signaling Pathways in the Management of Diabetes Mellitus - Focus on the Potential Role of GLP-1 Receptors Agonists and Selenium among Various Organ Systems.Current diabetes reviews · 2024Review
- Tanycytes control hypothalamic liraglutide uptake and its anti-obesity actions.Cell metabolism · 2022Article
- Emerging Nondopaminergic Medications for Parkinson's Disease: Focusing on A2A Receptor Antagonists and GLP1 Receptor Agonists.Journal of movement disorders · 2021Article
- The Capacity to Secrete Insulin Is Dose-Dependent to Extremely High Glucose Concentrations: A Key Role for Adenylyl Cyclase.Metabolites · 2021Article
- The ellagitannin metabolite urolithin C is a glucose-dependent regulator of insulin secretion through activation of L-type calcium channels.British journal of pharmacology · 2019Article
- Pleiotropic Effects of GLP-1 and Analogs on Cell Signaling, Metabolism, and Function.Frontiers in endocrinology · 2018Review
- GLP-1 receptor signalling promotes β-cell glucose metabolism via mTOR-dependent HIF-1α activation.Scientific reports · 2017Article
- Glucagon-Like Peptide-1 and Its Class B G Protein-Coupled Receptors: A Long March to Therapeutic Successes.Pharmacological reviews · 2016Review
- α/β-Hydrolase domain-6 and saturated long chain monoacylglycerol regulate insulin secretion promoted by both fuel and non-fuel stimuli.Molecular metabolism · 2015Article
- Beta cell connectivity in pancreatic islets: a type 2 diabetes target?Cellular and molecular life sciences : CMLS · 2015Review
- Glutamate acts as a key signal linking glucose metabolism to incretin/cAMP action to amplify insulin secretion.Cell reports · 2014Article
- Incretin-modulated beta cell energetics in intact islets of Langerhans.Molecular endocrinology (Baltimore, Md.) · 2014Article
- Article
- Insulin as a Bridge between Type 2 Diabetes and Alzheimer Disease - How Anti-Diabetics Could be a Solution for Dementia.Frontiers in endocrinology · 2014Review
- The permissive effects of glucose on receptor-operated potentiation of insulin secretion from mouse islets: a role for ERK1/2 activation and cytoskeletal remodelling.Diabetologia · 2013Article
- A role for cytosolic isocitrate dehydrogenase as a negative regulator of glucose signaling for insulin secretion in pancreatic ß-cells.PloS one · 2013Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundGlucagon like peptide-1 (GLP-1) and its analogue exendin-4 (Ex-4) enhance glucose stimulated insulin secretion (GSIS) and activate various signaling pathways in pancreatic beta-cells, in particular cAMP, Ca(2+) and protein kinase-B (PKB/Akt). In many cells these signals activate intermediary metabolism. However, it is not clear whether the acute amplification of GSIS by GLP-1 involves in part metabolic alterations and the production of metabolic coupling factors. METHODOLOGY/PRINICIPAL
findingsGLP-1 or Ex-4 at high glucose caused release (approximately 20%) of the total rat islet insulin content over 1 h. While both GLP-1 and Ex-4 markedly potentiated GSIS in isolated rat and mouse islets, neither had an effect on beta-cell fuel and energy metabolism over a 5 min to 3 h time period. GLP-1 activated PKB without changing glucose usage and oxidation, fatty acid oxidation, lipolysis or esterification into various lipids in rat islets. Ex-4 caused a rise in [Ca(2+)](i) and cAMP but did not enhance energy utilization, as neither oxygen consumption nor mitochondrial ATP levels were altered. CONCLUSIONS/SIGNIFICANCE: The results indicate that GLP-1 barely affects beta-cell intermediary metabolism and that metabolic signaling does not significantly contribute to GLP-1 potentiation of GSIS. The data also indicate that insulin secretion is a minor energy consuming process in the beta-cell, and that the beta-cell is different from most cell types in that its metabolic activation appears to be primarily governed by a "push" (fuel substrate driven) process, rather than a "pull" mechanism secondary to enhanced insulin release as well as to Ca(2+), cAMP and PKB signaling.
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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.