ArticlePloS one2022
A potent HNF4α agonist reveals that HNF4α controls genes important in inflammatory bowel disease and Paneth cells.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 13 citations in OpenAlex.
- Selective Influence of Hemp Fiber Ingestion on Post-Exercise Gut Permeability: A Metabolomics-Based Analysis.Nutrients · 2025Trial
- Temporal transcriptomic profiling identifies core regulators in cytokine-induced gut barrier disruption in differentiated Caco-2 cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- MetaLigand provides a prior-knowledge-guided framework for predicting non-peptide ligand mediated cell-cell communication.Cell reports methods · 2025Article
- Early subclinical stages of the inflammatory bowel diseases: insights from human and animal studies.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- Stress-induced mucin 13 reductions drive intestinal microbiome shifts and despair behaviors.Brain, behavior, and immunity · 2024Article
- Impact of various high fat diets on gene expression and the microbiome across the mouse intestines.Scientific reports · 2023Article
- Article
- TET2 and TET3 loss disrupts small intestine differentiation and homeostasis.Nature communications · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HNF4α has been implicated in IBD through a number of genome-wide association studies. Recently, we developed potent HNF4α agonists, including N-trans caffeoyltyramine (NCT). NCT was identified by structural similarity to previously the previously identified but weak HNF4α agonists alverine and benfluorex. Here, we administered NCT to mice fed a high fat diet, with the goal of studying the role of HNF4α in obesity-related diseases. Intestines from NCT-treated mice were examined by RNA-seq to determine the role of HNF4α in that organ. Surprisingly, the major classes of genes altered by HNF4α were involved in IBD and Paneth cell biology. Multiple genes downregulated in IBD were induced by NCT. Paneth cells identified by lysozyme expression were reduced in high fat fed mice. NCT reversed the effect of high fat diet on Paneth cells, with multiple markers being induced, including a number of defensins, which are critical for Paneth cell function and intestinal barrier integrity. NCT upregulated genes that play important role in IBD and that are downregulated in that disease. It reversed the loss of Paneth cell markers that occurred in high fat diet fed mice. These data suggest that HNF4α could be a therapeutic target for IBD and that the agonists that we have identified could be candidate therapeutics.
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