ArticleMolecular bioSystems2015
GC-MS metabolomics on PPARα-dependent exacerbation of colitis.
Article in Molecular bioSystems, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Translational Potential of Metabolomics on Animal Models of Inflammatory Bowel Disease-A Systematic Critical Review.International journal of molecular sciences · 2020Pooled it
- Metabolic Profiling of the Gut-Brain Axis in a Murine Model of Ulcerative Colitis with Raman Spectroscopy.ACS applied materials & interfaces · 2026Article
- Patient-derived colon epithelial organoids reveal lipid-related metabolic dysfunction in pediatric ulcerative colitis.Nature communications · 2025Article
- Malic enzyme 3 mediated the effects of malic acid on intestinal redox status and feed efficiency in broilers.Journal of animal science and biotechnology · 2025Article
- Anti-inflammatory role of fenofibrate in treating diseases.Biomolecules & biomedicine · 2023Review
- The PPARα Regulation of the Gut Physiology in Regard to Interaction with Microbiota, Intestinal Immunity, Metabolism, and Permeability.International journal of molecular sciences · 2022Review
- Mesenchymal stem cells-derived extracellular vesicles containing miR-378a-3p inhibit the occurrence of inflammatory bowel disease by targeting GATA2.Journal of cellular and molecular medicine · 2022Article
- Impact of purple sweet potato (RSC advances · 2022Article
- Artificial intelligence-rationalized balanced PPARα/γ dual agonism resets dysregulated macrophage processes in inflammatory bowel disease.Communications biology · 2022Article
- Impact of phytosterols on liver and distal colon metabolome in experimental murine colitis model: an explorative study.Journal of enzyme inhibition and medicinal chemistry · 2019Article
- Fecal metabolomic dataset of American ginseng-treated DSS mice: Correlation between ginseng enteric inflammation inhibition and its biological signatures.Data in brief · 2018Article
- rSj16 Protects against DSS-Induced Colitis by Inhibiting the PPAR-α Signaling Pathway.Theranostics · 2017Article
- A lipidomics investigation into the intervention of celastrol in experimental colitis.Molecular bioSystems · 2016Article
- Peroxisome proliferator-activated receptor (PPAR) α and δ activators induce ICAM-1 expression in quiescent non stimulated endothelial cells.Journal of inflammation (London, England) · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Fenofibrate, a peroxisome proliferator-activated receptor α (PPARα) agonist, was found to exacerbate inflammation and tissue injury in experimental acute colitis mice. Through lipidomics analysis, bioactive sphingolipids were significantly up-regulated in the colitis group. In this study, to provide further insight into the PPARα-dependent exacerbation of colitis, gas chromatography-mass spectrometry (GC/MS) based metabolomics was employed to investigate the serum and colon of dextran sulfate sodium (DSS)-induced colitis mice treated with fenofibrate, with particular emphasis on changes in low-molecular-weight metabolites. With the aid of multivariate analysis and metabolic pathway analysis, potential metabolite markers in the amino acid metabolism, urea cycle, purine metabolism, and citrate cycle were highlighted, such as glycine, serine, threonine, malic acid, isocitric acid, uric acid, and urea. The level changes of these metabolites in either serum or colons of colitis mice were further potentiated following fenofibrate treatment. Accordingly, the expression of threonine aldolase and phosphoserine aminotransferase 1 was significantly up-regulated in colitis mice and further potentiated in fenofibrate/DSS-treated mice. It was revealed that beyond the control of lipid metabolism, PPARα also shows effects on the above pathways, resulting in enhanced protein catabolism and energy expenditure, increased bioactive sphingolipid metabolism and proinflammatory state, which were possibly related to the exacerbated colitis.
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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.