ArticleThe Journal of physiology2011
Electrical activity-triggered glucagon-like peptide-1 secretion from primary murine L-cells.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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.
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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
54 citing papers in PubMed, 87 citations in OpenAlex.
- Calcium-Sensing Receptor Regulation of Gastrointestinal Hormone Secretion.Endocrine reviews · 2026Review
- Mechanisms and clinical implications of gut-brain interactions.The Journal of clinical investigation · 2026Review
- Article
- The Gut-Brain Axis in Parkinson disease: Emerging Concepts and Therapeutic Implications.Movement disorders clinical practice · 2025Review
- Integration of signal transduction pathways in sensory epithelial enteroendocrine cells.Molecular biology of the cell · 2025Review
- The gut-brain axis in early Parkinson's disease: from prodrome to prevention.Journal of neurology · 2025Review
- G Protein-Coupled Receptor 17 Inhibits Glucagon-like Peptide-1 Secretion via a Gi/o-Dependent Mechanism in Enteroendocrine Cells.Biomolecules · 2024Article
- Potassium voltage-gated channel subfamily H member 2 (KCNH2) is a promising target for incretin secretagogue therapies.Signal transduction and targeted therapy · 2024Article
- Cellular mechanisms of incretin hormone secretion.Journal of molecular endocrinology · 2024Review
- Kalium channelrhodopsins effectively inhibit neurons.Nature communications · 2024Article
- Article
- α-Synuclein expression in response to bacterial ligands and metabolites in gut enteroendocrine cells: anBrain communications · 2023Article
- Intestinal enteroendocrine cells rely on ryanodine and IPThe Journal of physiology · 2023Article
- Enteroendocrine cell regulation of the gut-brain axis.Frontiers in neuroscience · 2023Review
- The neural basis of sugar preference.Nature reviews. Neuroscience · 2022Review
- Specialized Mechanosensory Epithelial Cells in Mouse Gut Intrinsic Tactile Sensitivity.Gastroenterology · 2022Article
- Intestinal Gpr17 deficiency improves glucose metabolism by promoting GLP-1 secretion.Cell reports · 2022Article
- The gut-brain axis and Parkinson disease: clinical and pathogenetic relevance.Annals of medicine · 2021Review
- Input-output signal processing plasticity of vagal motor neurons in response to cardiac ischemic injury.iScience · 2021Article
- Glucose transporters in the small intestine in health and disease.Pflugers Archiv : European journal of physiology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Glucagon like peptide 1 (GLP-1) based therapies are now widely used for the treatment of type 2 diabetes. Developing our understanding of intestinal GLP-1 release may facilitate the development of new therapeutics aimed at targeting the GLP-1 producing L-cells. This study was undertaken to characterise the electrical activity of primary L-cells and the importance of voltage gated sodium and calcium channels for GLP-1 secretion. Primary murine L-cells were identified and purified using transgenic mice expressing a fluorescent protein driven by the proglucagon promoter. Fluorescent L-cells were identified within primary colonic cultures for patch clamp recordings. GLP-1 secretion was measured from primary colonic cultures. L-cells purified by flow cytometry were used to measure gene expression by microarray and quantitative RT-PCR. Electrical activity in L-cells was due to large voltage gated sodium currents, inhibition of which by tetrodotoxin reduced both basal and glutamine-stimulated GLP-1 secretion. Voltage gated calcium channels were predominantly of the L-type, Q-type and T-type, by expression analysis, consistent with the finding that GLP-1 release was blocked both by nifedipine and ω-conotoxin MVIIC. We observed large voltage-dependent potassium currents, but only a small chromanol sensitive current that might be attributable to KCNQ1. GLP-1 release from primary L-cells is linked to electrical activity and activation of L-type and Q-type calcium currents. The concept of an electrically excitable L-cell provides a basis for understanding how GLP-1 release may be modulated by nutrient, hormonal and pharmaceutical stimuli.
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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.