ArticleJCI insight2024
Glucose-dependent insulinotropic polypeptide receptor signaling alleviates gut inflammation in mice.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- The Possible Hematological Cost of Metabolic Success: Do Incretin-Based Therapies Silently Trigger Anemia?Medical sciences (Basel, Switzerland) · 2026Review
- Regulatory Role of Ribosome Biogenesis-Related Genes in Hepatocellular Carcinoma Prognosis and Construction of a Risk Prediction Model.Digestive diseases and sciences · 2026Article
- Altered GScience advances · 2026Article
- Disrupting the adiposopathy-inflammation loop: a translational immunometabolic framework for inflammatory disease.Journal of translational medicine · 2026Review
- Novel driver gene FIRRM regulates the cell cycle for promoting tumor growth in hepatocellular carcinoma.Journal of gastroenterology · 2026Article
- Peptide hormones and bile acids shaping immune tolerance of the liver: implications and applications.Protein & cell · 2026Review
- Tirzepatide mitigates atherosclerosis progression and modulates oxLDL-mediated proatherogenic effects in macrophages: evidence for M1/M2 homeostasis restoration.Archives of pharmacal research · 2026Article
- The role of the incretin GIP in inflammation.Journal of endocrinological investigation · 2026Review
- Loss of GLP-2R signaling in Glp2rMolecular metabolism · 2026Article
- Intestinal adaptation to cold-induced metabolic demand and feeding requires GLP-1R and GLP-2R signalling.Communications biology · 2025Article
- Antiinflammatory actions of glucagon-like peptide-1-based therapies beyond metabolic benefits.The Journal of clinical investigation · 2025 · on this mapReview
- Glucagon-like peptide-1 (GLP-1) receptor agonists in inflammatory bowel disease: mechanisms, clinical implications, and therapeutic potential.Journal of Crohn's & colitis · 2025Review
- Combined Use of Vitamin D and DPP-4 Inhibitors as a Potential Adjuvant Treatment Strategy to Enhance the Efficacy of Novel Beta-Cell Replacement Therapies for Type 1 Diabetes.Medical sciences (Basel, Switzerland) · 2025Review
- Review
- Gut Hormones and Inflammatory Bowel Disease.Biomolecules · 2025Review
- Therapeutic horizons in metabolic dysfunction-associated steatohepatitis.The Journal of clinical investigation · 2025Review
- Association between oral microbial diversity (only bacteria) and diabetes in U.S. adults: analysis of NHANES 2009-2012 data.BMC oral health · 2025Article
- Bidirectional Interactions Between the Gut Microbiota and Incretin-Based Therapies.Life (Basel, Switzerland) · 2025Review
- Unveiling the Therapeutic Potential of the Second-Generation Incretin Analogs Semaglutide and Tirzepatide in Type 1 Diabetes and Latent Autoimmune Diabetes in Adults.Journal of clinical medicine · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are gut-derived peptide hormones that potentiate glucose-dependent insulin secretion. The clinical development of GIP receptor-GLP-1 receptor (GIPR-GLP-1R) multiagonists exemplified by tirzepatide and emerging GIPR antagonist-GLP-1R agonist therapeutics such as maritide is increasing interest in the extrapancreatic actions of incretin therapies. Both GLP-1 and GIP modulate inflammation, with GLP-1 also acting locally to alleviate gut inflammation in part through antiinflammatory actions on GLP-1R+ intestinal intraepithelial lymphocytes. In contrast, whether GIP modulates gut inflammation is not known. Here, using gain- and loss-of-function studies, we show that GIP alleviates 5-fluorouracil-induced (5FU-induced) gut inflammation, whereas genetic deletion of Gipr exacerbates the proinflammatory response to 5FU in the murine small bowel (SB). Bone marrow (BM) transplant studies demonstrated that BM-derived Gipr-expressing cells suppress 5FU-induced gut inflammation in the context of global Gipr deficiency. Within the gut, Gipr was localized to nonimmune cells, specifically stromal CD146+ cells. Hence, the extrapancreatic actions of GIPR signaling extend to the attenuation of gut inflammation, findings with potential translational relevance for clinical strategies modulating GIPR action in people with type 2 diabetes or obesity.
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