ArticleGastroenterology2006
Bile acids induce ileal damage during experimental necrotizing enterocolitis.
Article in Gastroenterology, 2006. 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.
The trial behind it
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, 97 citations in OpenAlex.
- Necrotizing enterocolitis is exacerbated through SUCNR1/HIF-1α/BNIP3 axis-mediated succinate-induced intestinal epithelial cell apoptosis.Pediatric research · 2026Article
- Sodium butyrate protects against necrotizing enterocolitis through a mechanism involving YB-1-dependent regulation of intestinal epithelial apoptosis.Scientific reports · 2026Article
- Disruption of bile acid homeostasis potentiates Paneth cell ablation by activating the intestinal Farnesoid X receptor in necrotizing enterocolitis.NPJ biofilms and microbiomes · 2026Article
- Succinate Promotes M1 Polarization of Intestinal Macrophages in Mice With Necrotizing Enterocolitis Through the PI3K/AKT Pathway.Pediatric discovery · 2025Article
- Review: microbial metabolites - a key to address gut inflammation and barrier dysfunction in the premature infant.Gut microbes · 2025Review
- Gut Microbiota-Derived Metabolites and Their Role in the Pathogenesis of Necrotizing Enterocolitis in Preterm Infants: A Narrative Review.Metabolites · 2024Review
- Metabolic immaturity and breastmilk bile acid metabolites are central determinants of heightened newborn vulnerability to norovirus diarrhea.Cell host & microbe · 2024Article
- Extracellular Nicotinamide Phosphoribosyltransferase Is a Therapeutic Target in Experimental Necrotizing Enterocolitis.Biomedicines · 2024Article
- Deoxycholic acid aggravates necrotizing enterocolitis through downregulation of mesenchymal-epithelial transition factor expression.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Targeted LC-MS/MS profiling of bile acids reveals primary/secondary bile acid ratio as a novel biomarker for necrotizing enterocolitis.Analytical and bioanalytical chemistry · 2024Article
- Article
- Enteral Feeding and Antibiotic Treatment Do Not Influence Increased Coefficient of Variation of Total Fecal Bile Acids in Necrotizing Enterocolitis.Newborn (Clarksville, Md.) · 2023Article
- The inhibition of enterocyte proliferation by lithocholic acid exacerbates necrotizing enterocolitis through downregulating the Wnt/β-catenin signalling pathway.Cell proliferation · 2022Article
- Crosstalk Between the Gut Microbiota and Epithelial Cells Under Physiological and Infectious Conditions.Frontiers in cellular and infection microbiology · 2022Review
- Succinate aggravates intestinal injury in mice with necrotizing enterocolitis.Frontiers in cellular and infection microbiology · 2022Article
- Chorioamnionitis induces hepatic inflammation and time-dependent changes of the enterohepatic circulation in the ovine fetus.Scientific reports · 2021Article
- Review
- Article
- Intestinal Absorption of Bile Acids in Health and Disease.Comprehensive Physiology · 2019Review
- A novel bioluminescence-based method to investigate uptake of bile acids in living cells.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsNecrotizing enterocolitis (NEC) is the most common gastrointestinal emergency of premature infants. While the effect of bile acids (BAs) on intestinal mucosal injury is known, we investigated the contribution of BAs during the development of NEC in neonatal rats.
methodsPremature rats were fed with cow's milk-based formula and subjected to asphyxia and cold stress to develop NEC. Jejunal and ileal luminal BAs, portal blood BAs, and messenger RNA and protein for the apical sodium-dependent bile acid transporter, the ileal bile acid binding protein, and the heteromeric organic solute transporter (Ostalpha/Ostbeta)were evaluated.
resultsIleal luminal BAs levels were increased significantly during disease development and the removal of ileal BAs significantly decreased the incidence and severity of disease. Furthermore, when NEC was reduced via treatment with epidermal growth factor (EGF), BA levels were reduced significantly. Jejunal luminal BA levels were similar between animals with NEC and controls, but portal/ileal luminal BA ratios were decreased significantly in animals with NEC. The apical sodium-dependent bile acid transporter was up-regulated at the site of injury in animals with NEC and decreased after EGF treatment; however, the ileal bile acid binding protein was up-regulated only in the NEC and EGF group. Ostalpha/Ostbeta expression was low in all groups, and only slightly increased in the NEC group.
conclusionsThese data strongly suggest that BAs play a role in the development of ileal damage in experimental NEC and that alterations in BA transport in the neonatal ileum may contribute to disease development.
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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.