ArticleEndocrinology2011
Mechanism of action of glucagon-like peptide-2 to increase IGF-I mRNA in intestinal subepithelial fibroblasts.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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
29 citing papers in PubMed, 69 citations in OpenAlex.
- GLP-1 and GLP-2 as intestinal reparative therapies in inflammatory bowel disease: mechanisms, translation, and clinical opportunity.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- TSLP links intestinal nutrient sensing with amplification of the ILC2-tuft cell circuit.Nature immunology · 2025Article
- Gut Hormones and Inflammatory Bowel Disease.Biomolecules · 2025Review
- Activation of VEGFR3 and MLC2 are Critical for GLP-2 Enhancement of Chylomicron Transport.Gastro hep advances · 2025Article
- Review
- The intestine as an endocrine organ and the role of gut hormones in metabolic regulation.Nature reviews. Gastroenterology & hepatology · 2023Review
- Prognostic model development for classification of colorectal adenocarcinoma by using machine learning model based on feature selection technique boruta.Scientific reports · 2023Article
- Article
- Intra-amniotic administration of l-glutamine promotes intestinal maturation and enteroendocrine stimulation in chick embryos.Scientific reports · 2022Article
- Perspective: Prospects for Nutraceutical Support of Intestinal Barrier Function.Advances in nutrition (Bethesda, Md.) · 2021Article
- GLP-2, EGF, and the Intestinal Epithelial IGF-1 Receptor Interactions in the Regulation of Crypt Cell Proliferation.Endocrinology · 2020Article
- Control of Intestinal Epithelial Proliferation and Differentiation: The Microbiome, Enteroendocrine L Cells, Telocytes, Enteric Nerves, and GLP, Too.Digestive diseases and sciences · 2019Article
- The roles of glucagon-like peptide-2 and the intestinal epithelial insulin-like growth factor-1 receptor in regulating microvillus length.Scientific reports · 2019Article
- Neuropods.Cellular and molecular gastroenterology and hepatology · 2019Review
- Glucagon-Like Peptide-2 and the Enteric Nervous System Are Components of Cell-Cell Communication Pathway Regulating Intestinal NaFrontiers in nutrition · 2018Article
- Tissue Engineering Functional Gastrointestinal Regions: The Importance of Stem and Progenitor Cells.Cold Spring Harbor perspectives in medicine · 2017Review
- Interdependency of EGF and GLP-2 Signaling in Attenuating Mucosal Atrophy in a Mouse Model of Parenteral Nutrition.Cellular and molecular gastroenterology and hepatology · 2017Article
- Generation of glucagon-like peptide-2-expressing Saccharomyces cerevisiae and its improvement of the intestinal health of weaned rats.Microbial biotechnology · 2016Article
- Temporal and Regional Expression of Glucose-Dependent Insulinotropic Peptide and Its Receptor in Spinal Cord Injured Rats.Journal of neurotrauma · 2016Article
- Glucagon-like peptide-2 protects impaired intestinal mucosal barriers in obstructive jaundice rats.World journal of gastroenterology · 2015Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
IGF-I, a known secretory product of intestinal subepithelial myofibroblasts (ISEMFs), is essential for the intestinotropic effects of glucagon-like peptide-2 (GLP-2). Furthermore, GLP-2 increases IGF-I mRNA transcript levels in vitro in heterogeneous fetal rat intestinal cultures, as well as in vivo in the rodent small intestine. To determine the mechanism underlying the stimulatory effect of GLP-2 on intestinal IGF-I mRNA, murine ISEMF cells were placed into primary culture. Immunocytochemistry showed that the ISEMF cells appropriately expressed α-smooth muscle actin and vimentin but not desmin. The cells also expressed GLP-2 receptor and IGF-I mRNA transcripts. Treatment of ISEMF cells with (Gly2)GLP-2 induced IGF-I mRNA transcripts by up to 5-fold of basal levels after treatment with 10(-8) m GLP-2 for 2 h (P < 0.05) but did not increase transcript levels for other intestinal growth factors, such as ErbB family members. Immunoblot revealed a 1.6-fold increase in phospho (p)-Akt/total-(t)Akt with 10(-8) m GLP-2 treatment (P < 0.05) but no changes in cAMP, cAMP-dependent β-galactosidase expression, pcAMP response element-binding protein/tcAMP response element-binding protein, pErk1/2/tErk1/2, or intracellular calcium. Furthermore, pretreatment of ISEMF cells with the phosphatidylinositol 3 kinase (PI3K) inhibitors, LY294002 and wortmannin, abrogated the IGF-I mRNA response to GLP-2, as did overexpression of kinase-dead Akt. The role of PI3K/Akt in GLP-2-induced IGF-I mRNA levels in the murine jejunum was also confirmed in vivo. These findings implicate the PI3K/Akt pathway in the stimulatory effects of GLP-2 to enhance intestinal IGF-I mRNA transcript levels and provide further evidence in support of a role for IGF-I produced by the ISEMF cells in the intestinotropic effects of GLP-2.
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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.