ArticleEndocrinology2012
Regulation of mouse intestinal L cell progenitors proliferation by the glucagon family of peptides.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Molecular Mechanisms of Intestinal Adaptation in Short Bowel Syndrome: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Intestinal adaptation to cold-induced metabolic demand and feeding requires GLP-1R and GLP-2R signalling.Communications biology · 2025Article
- p21-Activated Kinase 1 (Pak1) as an Element in Functional and Dysfunctional Interplay Among the Myocardium, Adipose Tissue, and Pancreatic Beta Cells.Comprehensive Physiology · 2025Review
- Ligands for Intestinal Intraepithelial T Lymphocytes in Health and Disease.Pathogens (Basel, Switzerland) · 2025Review
- P21-activated kinase-1 signaling is required to preserve adipose tissue homeostasis and cardiac function.Molecular and cellular biochemistry · 2025Article
- The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Glucagon Acting at the GLP-1 Receptor Contributes to β-Cell Regeneration Induced by Glucagon Receptor Antagonism in Diabetic Mice.Diabetes · 2023Article
- Distinct Identity of GLP-1R, GLP-2R, and GIPR Expressing Cells and Signaling Circuits Within the Gastrointestinal Tract.Frontiers in cell and developmental biology · 2021Review
- Glucagon receptor antagonist upregulates circulating GLP-1 level by promoting intestinal L-cell proliferation and GLP-1 production in type 2 diabetes.BMJ open diabetes research & care · 2020Article
- Glucagon-Like Peptide-1 Secreting L-Cells Coupled to Sensory Nerves Translate Microbial Signals to the Host Rat Nervous System.Frontiers in cellular neuroscience · 2020Article
- Neonatal Consumption of Oligosaccharides Greatly Increases L-Cell Density without Significant Consequence for Adult Eating Behavior.Nutrients · 2019Article
- Does GLP-1 suppress its own basal secretion?Endocrine research · 2016Article
- Angptl4 links α-cell proliferation following glucagon receptor inhibition with adipose tissue triglyceride metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Glucagon receptor antagonism induces increased cholesterol absorption.Journal of lipid research · 2015Article
- Lack of glucagon receptor signaling and its implications beyond glucose homeostasis.The Journal of endocrinology · 2015Review
- Mouse insulin cells expressing an inducible RIPCre transgene are functionally impaired.The Journal of biological chemistry · 2015Article
- Incretin receptor null mice reveal key role of GLP-1 but not GIP in pancreatic beta cell adaptation to pregnancy.PloS one · 2014Article
- Novel insight into the distribution of L-cells in the rat intestinal tract.American journal of translational research · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Glucagon like peptide-1 (GLP-1) and GLP-2 are hormones secreted by intestinal L cells that stimulate glucose-dependent insulin secretion and regulate intestinal growth, respectively. Mice with deletion of the glucagon receptor (Gcgr) have high levels of circulating GLP-1 and GLP-2. We sought to determine whether the increased level of the glucagon-like peptides is due to L cell hyperplasia. We found, first, that high levels of the glucagon-like peptides increase L cell number but does not affect the number of other intestinal epithelial cell types. Second, a large proportion of ileal L cells of Gcgr(-/-) mice coexpressed glucose-dependent insulinotropic peptide (GIP). Cells coexpressing GIP and GLP-1 are termed LK cells. Third, the augmentation in L cell number was due to a higher rate of proliferation of L cell progenitors rather than to the entrance of mature L cells into the cell cycle. Fourth, a high concentration of the glucagon-like peptides in the circulation augmented the mRNA levels of transcription factors expressed by late but not early enteroendocrine progenitors. Fifth, the administration of exendin 9-39, a GLP-1 receptor antagonist, resulted in a decrease in the rate of L cell precursor proliferation. Finally, we determined that L cells do not express the GLP-1 receptor, suggesting that the effect of GLP-1 is mediated by paracrine and/or neuronal signals. Our results suggest that GLP-1 plays an important role in the regulation of L cell number.
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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.