ArticleScientific reports2017
GLP-1 receptor signalling promotes β-cell glucose metabolism via mTOR-dependent HIF-1α activation.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 122 citations in OpenAlex.
- GIP and GLP-1 Potentiate Sulfonylurea-Induced Insulin Secretion in Hepatocyte Nuclear Factor 1α Mutation Carriers.Diabetes · 2020Trial
- Glucagon-Like Peptide-1 Receptor Agonist Use Before and After Liver Transplant.Gastroenterology & hepatology · 2026Article
- Metabolic breakdown: Linking insulin resistance and mitochondrial dysfunction to neurodegeneration in Alzheimer's disease.Neural regeneration research · 2026Article
- Med14 phosphorylation shapes genomic response to GLP-1 agonists.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Clinical Impact of Semaglutide Beyond Glycemic Control: A Critical Analysis of Oncogenic Potential and Mitigation of Cardiotoxicity.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Lysolecithin reprogramming via LPCAT1 modulation restores endothelial function and prevents diabetes-associated dysmetabolism.Cardiovascular diabetology · 2026Article
- The Intricate Interplay of Noncoding RNAs and the Gut Microbiome in Gastrointestinal and Endocrine-Related Cancers.Sub-cellular biochemistry · 2026Review
- Glucagon-Like Peptide-1: The Role of Calcium in Gut-Glucose Axis.Advances in experimental medicine and biology · 2026Review
- GLP-1R associates with VAPB and SPHKAP at ERMCSs to regulate β-cell mitochondrial remodelling and function.Nature communications · 2025Article
- Integrative gene-metabolite network analysis of GLP-1 receptor agonists and related incretin pathways in cardiometabolic health.NPJ systems biology and applications · 2025Article
- Roles of glucagon-like peptide 1 receptor agonists in immune cell biology and autoimmune/autoinflammatory diseases.Cell & bioscience · 2025Review
- Exendin-4 enhances insulin-positive phenotype of human pluripotent stem cell-derived β cells during transplantation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics.Nature communications · 2025Article
- Semaglutide-induced weight loss improves mitochondrial energy efficiency in skeletal muscle.Obesity (Silver Spring, Md.) · 2025Article
- Metabolic interplays between the tumour and the host shape the tumour macroenvironment.Nature reviews. Cancer · 2025Review
- Dysregulation of Metabolic Peptides in the Gut-Brain Axis Promotes Hyperinsulinemia, Obesity, and Neurodegeneration.Biomedicines · 2025Review
- The role of hypoxia-inducible factors 1 and 2 in the pathogenesis of diabetic kidney disease.Journal of nephrology · 2025Review
- Tryptophan metabolism at the crossroads of the neuro-immuno-microbial axis: implications for precision medicine in chronic diseases.Frontiers in cellular and infection microbiology · 2025Review
- 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
- The Physiological Functions and Therapeutic Potential of Hypoxia-Inducible Factor-1α in Vascular Calcification.Biomolecules · 2024Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucagon-like peptide-1 (GLP-1) promotes insulin secretion from pancreatic β-cells in a glucose dependent manner. Several pathways mediate this action by rapid, kinase phosphorylation-dependent, but gene expression-independent mechanisms. Since GLP-1-induced insulin secretion requires glucose metabolism, we aimed to address the hypothesis that GLP-1 receptor (GLP-1R) signalling can modulate glucose uptake and utilization in β-cells. We have assessed various metabolic parameters after short and long exposure of clonal BRIN-BD11 β-cells and rodent islets to the GLP-1R agonist Exendin-4 (50 nM). Here we report for the first time that prolonged stimulation of the GLP-1R for 18 hours promotes metabolic reprogramming of β-cells. This is evidenced by up-regulation of glycolytic enzyme expression, increased rates of glucose uptake and consumption, as well as augmented ATP content, insulin secretion and glycolytic flux after removal of Exendin-4. In our model, depletion of Hypoxia-Inducible Factor 1 alpha (HIF-1α) impaired the effects of Exendin-4 on glucose metabolism, while pharmacological inhibition of Phosphoinositide 3-kinase (PI3K) or mTOR completely abolished such effects. Considering the central role of glucose catabolism for stimulus-secretion coupling in β-cells, our findings suggest that chronic GLP-1 actions on insulin secretion include elevated β-cell glucose metabolism. Moreover, our data reveal novel aspects of GLP-1 stimulated insulin secretion involving de novo gene expression.
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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.