ArticleJournal of pediatric surgery2014
Insulin-like growth factor 2 and its enterocyte receptor are not required for adaptation in response to massive small bowel resection.
Article in Journal of pediatric surgery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Molecular Mechanisms of Intestinal Adaptation in Short Bowel Syndrome: A Comprehensive Review.International journal of molecular sciences · 2026Review
- The Effect ofLife (Basel, Switzerland) · 2022Article
- Host-Gut Microbiota Crosstalk in Intestinal Adaptation.Cellular and molecular gastroenterology and hepatology · 2018Review
- Epithelial IGF1R is dispensable for IGF2 mediated enhanced intestinal adaptation in retinoblastoma-deficient mice.Journal of pediatric surgery · 2017Article
- The Pathogenesis of Resection-Associated Intestinal Adaptation.Cellular and molecular gastroenterology and hepatology · 2016Review
- Mechanisms of intestinal adaptation.Best practice & research. Clinical gastroenterology · 2016Review
- Both epidermal growth factor and insulin-like growth factor receptors are dispensable for structural intestinal adaptation.Journal of pediatric surgery · 2015Article
- High-protein diet improves postoperative weight gain after massive small-bowel resection.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2015Article
- Early-onset metabolic syndrome in mice lacking the intestinal uric acid transporter SLC2A9.Nature communications · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeEnhanced structural features of resection-induced intestinal adaptation have been demonstrated following the administration of multiple different growth factors and peptides. Among these, the insulin-like growth factor (IGF) system has been considered to be significant. In this study, we employ mutant mouse strains to directly test the contribution of IGF2 and its enterocyte receptor (IGF1R) toward the adaptation response to massive small bowel resection (SBR).
methodsIGF2-knockout (IGF2-KO) (n=8) and intestine specific IGF1R-knockout mice (IGF1R-IKO) (n=9) and their wild type (WT) littermates (n=5, n=7, respectively) underwent 50% proximal SBR. At post-operative day 7, structural adaptation was measured as crypt depth and villus height. Rates of enterocyte proliferation and apoptosis were also recorded.
resultsThe successful deletion of IGF2 and IGF1R expression in the enterocytes was confirmed by RT-PCR and Western blot, respectively. Normal adaptation occurred in both IGF2-KO and IGF1R-IKO mice after 50% SBR. Post-operative rates of proliferation and apoptosis in both IGF2-KO and IGF1R-IKO mice were no different than their respective controls.
conclusionIGF2 and functional IGF1R signaling in enterocytes are both dispensable for resection-induced adaptation responses. The mechanism for IGF-stimulation of intestinal adaptation may involve other ligands or cellular compartments within the intestine.
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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.