Abstract
Interactions between the host, diet and intestinal microbiota are critical for metabolic and immune homeostasis, but the intersecting metabolites and receptors remain poorly defined. Here we identify 10-oxostearic acid (10-oxoSA), a microbial metabolite derived from oleic acid, the most abundant fatty acid in nature, as a potent and selective agonist of the lipid-sensing nuclear receptor peroxisome proliferator-activated receptor alpha (PPARα). Biochemical and structural analyses reveal that 10-oxoSA binds PPARα with higher affinity than previously identified endogenous ligands. In a mouse model of colitis, 10-oxoSA confers protection in a PPARα-dependent manner. Multi-tissue transcriptomics show that 10-oxoSA upregulates beneficial PPARα target genes in the ileum and colon, many in previously unrecognized pathways, while also circumventing deleterious hepatic responses. Multi-omics analyses also show that prolonged oral 10-oxoSA administration is well tolerated in the gut and liver with minimal impact on gut microbiota composition. These findings establish a natural diet–microbiota–host axis with potential for anti-inflammatory interventions.
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Data availability
Metabolomic data that support the findings of this study have been deposited in MassIVE with ID MSV000097676. Protein structures used in this study have been deposited in PDB under codes 9VZT, 9VZS, 6LX7 and 6KAZ. Raw RNA-seq data (project accession number PRJNA1256500) and raw sequences of metagenomics (project accession number PRJNA1256330) have been deposited in the NCBI Sequence Read Archive. The SPARC IBD dataset is available upon request and subject to approval. Researchers can contact Angela Dobes (adobes@crohnscolitisfoundation.org) at the Crohn’s & Colitis Foundation. Requests can generally be addressed immediately upon receipt. Source data are provided with this paper.
Code availability
Code used in pull-down analyses is available via GitHub at https://github.com/huiUofT/eCPIN.
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Acknowledgements
We acknowledge the experimental assistance of V. Dhar and K. Khanna from the Department of Microbiology at New York University Langone Health (New York, USA) during data collection, and M. A. Fragoso García from the Histology & Comparative Pathology Core at the Albert Einstein College of Medicine (New York, USA) for generating the histological images and helping to verify the histological scores. J.L. was supported by a Charles H. Best Postdoctoral Fellowship and Precision Medicine Initiative Fellowship. Work performed was supported by a Canadian Institutes of Health Research grant (PJT-186117) to H.M.K.; a New Frontiers in Research Fund grant (NRFRE-2019-00901) to H.M.K., C.L.C. and H.P.; a Japan Agency for Medical Research and Development grant (JP21am0101071) to S.K. and I.I.; a National Natural Science Foundation of China grant (82204227, 82574272) to X.W.; and a Science and Technology Development Fund, Macau SAR grant (0002/2025/NPR) to S.W. The work was performed in part using internal funds for the purchase of faecal data samples: National Cancer Institute, Cancer Center Support Grant 31094N and Donation Fund 305613 Project Award, Albert Einstein College of Medicine, Bronx, NY. The results published here are partly based on data and biosamples from the Study of a Prospective Adult Research Cohort with IBD (SPARC IBD). SPARC IDB is a component of the Crohn’s & Colitis Foundation’s IBD Plexus data exchange platform.
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J.L. designed and performed the research experiments, analysed data and wrote the paper. H.L., Y.T., M.G., C.S., S.K., A.H., J.S., E.D.Y. and J.C. performed the research. M.J. performed the bioinformatics analyses. D.Y. and Y.G. assisted in LC–MS analysis. S.H. assisted in animal studies. W.N., I.I., C.L.C., H.P. and S.W. designed the experiments and made manuscript revisions. X.W., S.M. and H.M.K. designed the research and wrote the manuscript. All authors reviewed the final manuscript.
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Extended data
Extended Data Fig. 1 Comparison of chromatograms of standard 10-oxoSA and 10-HSA and representative pull-down samples.
a Volcano plot of differential ions enriched by PPARα or FXR in stools of IBD patients. P values were calculated using an unpaired two-tailed t-test. Horizontal dash indicates p value < 0.05; vertical dash indicates |fold change | > 2. Data are provided in the Supplementary Table 2. b Top panels are extracted-ion chromatograms (EICs) of standard 10-oxoSA and 10-HSA. The remaining are representative EICs of 10-oxoSA and 10-HSA (m/z 297.2435, and 299.2591) pulled down by PPARα and FXR.
Extended Data Fig. 2 Validation of 10-oxoSA and 10-HSA bound with PPARα-LBD and analyses of ligand interactions with PPARα.
a 10-oxoSA and 10-HSA stabilize the PPARα-LBD as shown using a fluorescent thermal shift assay (n = 3). b–d HEK293 cells were transfected with GAL4-hPPAR-LBDs and UAS luciferase constructs and then treated with 10-oxoSA,10-HSA, or corresponding positive controls for 16 hours. Absolute luciferase units were normalized to β-galactosidase activity and then multiplied by incubation time after addition of β-galactosidase buffer. Data are expressed as means ± SD (n = 3 technical replicates). 2 independent biological replicates per group. Protein expression levels are provided in the Source Data file. e Protein expression levels of Gal4-PPARα, Gal4-PPARβ, and Gal4-PPARγ in the transfected HEK293 cells measured by immunoblotting. β-Actin was used as the loading control. Experiments were performed in triplicate and repeated twice with similar results. f–i Crystal structure of agonist-bound PPARα-LBD and its molecular and functional analyses. Magnified views of steric acid (f), 10-oxoSA (g), 10-HSA (h), and pemafibrate (i) in the PPARα-LBD cocrystal. j 10-Hydroxy R-configuration of 10-HSA. k Functional effects of mutations in the potential binding residues on transcriptional activity. Wild-type (WT) and mutant constructs (T279A or T279S) were examined by luciferase reporter assay with pemafibrate (1 μM), 10-HSA (10 μM), or 10-oxoSA (10 μM). The mutant constructs show a significant reduction in PPARα’s transcriptional activity. n = 3 independent experiments, Data are presented as mean ± SD. p values were calculated using one-way ANOVA compared with agonist-treated WT. l Mutations do not affect protein expression levels. β-Actin was used as the loading control. Experiments were performed in triplicate and repeated twice with similar results. Source data are provided in the Source Data file.
Extended Data Fig. 3 Effects on mouse PPARα transcriptional activity.
HEK293 cells were transfected with GAL4-mPPAR-LBDs and UAS luciferase constructs and then treated with (a) 10-oxoSA or (b) 10-HSA for 16 hours. Absolute luciferase units were normalized to β-galactosidase activity and then multiplied by incubation time after addition of β-galactosidase buffer. Data are expressed as means ± SD (n = 3 technical replicates). Three independent experiments per group. Source data are provided in the Source Data file.
Extended Data Fig. 4 10-oxoSA alleviates DSS-induced colitis.
WT female mice were challenged with DSS for 9 days and treated with DMSO (Vehicle) or 10-oxoSA administered by oral and rectal gavage (n = 12). a Colonic PPARα expression levels. b Disease activity index. c Body weight changes during DSS. d Colon length shortening. e Microphotographs of H&E stained sections of colons. Images are acquired at 2.5× magnification, with the inlets shown at 10× magnification. Scale bar: 100 μm. n = 3 biological samples per group, the representative example shown. f Histological score. b,c Each data point represents a biological replicate and is presented as mean ± SD (n = 12). d,f Each data point represents a biological replicate and is presented as mean ± SD (n = 8). P values were calculated using an one-way ANOVA compared with DSS group (b–d, f). Source data are provided in the Source Data file.
Extended Data Fig. 5 Acute supplementation of 10-oxoSA alleviates colitis in male mice.
WT male mice challenged with DSS and treated with DMSO (Vehicle) or 10-oxoSA by oral and rectal gavage were tested for body weight loss rate (a), colon length shortening (b), histological score (c), H&E analysis (d). Scale bars, 100 μm. Each data point represents a biological replicate and is presented as mean ± SD (n = 8). P values were calculated using an unpaired two-tailed t-test. Source data are provided in the Source Data file.
Extended Data Fig. 6 Levels of 10-oxoSA and 10-HSA in stools and effects on colitis mice.
a,b Quantification of 10-HSA (a) and 10-oxoSA (b) in stools from DSS-induced colitis mice treated with DMSO (vehicle), 10-HSA, and 10-oxoSA (n = 16) at day 0 and day 10 using LC-MS2. c,d Quantification of 10-HSA (c) and 10-oxoSA (d) in stools from DSS-induced colitis Ppara KO mice treated with DMSO (vehicle) or 10-oxoSA (n = 12) at day 0 and day 8 using LC-MS2. P values were calculated using a two-way ANOVA with multiple comparisons test. Source data are provided in the Source Data file.
Extended Data Fig. 7 Altered gene expression in colon.
a Hallmark signatures identified from GSEA in the colon, ordered by p value (Padjust). GSEA was performed for KEGG pathway enrichment. b GSEA plots of differentially expressed genes in the colons of mice supplemented with 10-oxoSA for 6 weeks (n = 3) compared to those supplemented with the vehicle (n = 3), for Epithelial-Mesenchymal Transition, Interferon Alpha Response, Interferon Gamma Response, and Angiogenesis. GSEA was conducted using a Kolmogorov-Smirnov test. Top of the plot indicates the direction of enrichment. The green curve represents the enrichment score (ES), a running-sum statistic calculated as the analysis walks down the ranked list of genes. The curve peak represents the ES for the gene set. Enrichment toward the right suggests upregulation in the vehicle-treated colon. Vertical black lines indicate the positions of genes from the selected gene set in the ranked list, representing the ‘hits’ that contribute to the ES. The gray background represents the full ranked gene list based on the correlation with the 10-oxoSA-treatment or vehicle. GSEA gene set enrichment analysis. NES normalized enrichment score.
Extended Data Fig. 8 Altered gene expression in ileum.
a Volcano plot of differential gene expression in the ileum after 10-oxoSA (n = 3) or vehicle treatment (n = 3). Orange dots indicate differentially expressed genes with statistically significant change (fold change > 2, padjust < 0.05). Blue dots indicate differentially expressed genes with statistically significant change (1< fold change < 2, padjust < 0.05). b KEGG enrichment analysis highlighting pathways in the ileum of mice treated with 10-oxoSA for 6 weeks compared to vehicle treatment. The size of circle on the left for each gene represents the fold change (log2FC) of 10-oxoSA treatment compared to vehicle treatment. The enriched pathways are categorized into different pathway groups based on the KEGG pathway database. The size of circle on the right for each pathway represents counts of enriched genes. Counts are Z-score normalized. n = 3 sample per group. a,b P values for RNASeq data were calculated using general linear model with negative binomial distribution. c Hallmark signatures identified from GSEA in the ileum, ordered by p value (Padjust). GSEA was performed for KEGG pathway enrichment. d GSEA plots of differentially expressed genes in the ileums of mice supplemented with 10-oxoSA for 6 weeks (n = 3) compared to those supplemented with vehicle (n = 3), for Adipogenesis, Xenobiotic Metabolism, Fatty Acid Metabolism, and Bile Acid Metabolism. Top of the plot indicates the direction of enrichment. Green curve represents the enrichment score (ES), a running-sum statistic calculated as the analysis walks down the ranked list of genes. The curve peak represents the ES for the gene set. Enrichment toward the left suggests upregulation in the 10-oxoSA-treated colon. Vertical black lines indicate the positions of genes from the selected gene set in the ranked list, representing the ‘hits’ that contribute to the ES. The gray background represents the full ranked gene list based on the correlation with the 10-oxoSA-treatment or vehicle. GSEA was conducted using a Kolmogorov-Smirnov test. GSEA gene set enrichment analysis. NES normalized enrichment score.
Extended Data Fig. 9 10-oxoSA effects in liver.
a Liver-to-body weight ratios in treated mice. b Liver weights in treated mice. c Body weights in treated mice. a–c n = 11 for vehicle supplemented mice, and n = 12 for 10-oxoSA supplemented mice. Data are expressed as means ± SD; P values were calculated using a two-tailed Student’s t-test. d H&E staining of the liver from acute UC mice. Scale bar = 100 μm. n = 3 mice, biological samples per group, a representative example is shown. GSEA Gene Set Enrichment Analysis. e Volcano plot of differential gene expression in the liver after 10-oxoSA (n = 3) or vehicle (n = 3) treatment. Orange dots indicate differentially expressed genes with statistically significant change (fold change > 2, padjust < 0.05). Blue dots indicate differentially expressed genes with statistically significant change (1< fold change < 2, padjust < 0.05). f KEGG enrichment analysis highlighting pathways in the liver of mice treated with 10-oxoSA for 6 weeks compared to vehicle treatment. The size of circle on the left for each gene represents the fold change (log2FC) after 10-oxoSA treatment versus vehicle treatment. Enriched pathways are categorized into different pathway groups based on the KEGG pathway database. The size of circle on the right for each pathway represents counts of enriched genes. Counts are Z-score normalized. n = 3 sample per group. e,f P values for RNASeq data were calculated using general linear model with negative binomial distribution. Source data are provided in the Source Data file.
Extended Data Fig. 10 10-oxoSA effects on bacteria growth and 10-oxoSA production.
a Relative fecal bacterial abundance (n = 11 for Vehicle, n = 12 for 10-oxoSA). Data are expressed as means ± SD. P values were calculated using a two-sided Wilcoxon rank-sum test. Green indicates the species inhibited by 10-oxoSA. Red indicates the species promoted by 10-oxoSA. b,c Growth of representative A. muciniphila, L. reuteri NM11, L. reuteri NM12 and L. johnsonii NM60 strains supplemented with 150 μg/ml of 10-oxoSA. F. prausnitzii, R. gnavus, and C. scindens are controls. n = 4 for A. muciniphila, F. prausnitzii, R. gnavus, and C. scindens, n = 6 for L. reuteri NM11, and L. reuteri NM12, n = 5 for L. johnsonii NM60. Data were analyzed by two-way ANOVA with multiple comparisons and are expressed as mean ± SD. d,e Evaluation of 10-oxoSA, and 10-HSA producing ability across a 27-strain lactobacilli collection. Lactobacilli strains were incubated for 48 hours with (d) OA (500 µM) or (e) LA (500 µM) in MRS broth, and the negative control without OA (n = 3 technical replicates). Values were normalized to bacterial cell density by OD600 and corrected by subtraction of the negative control value. Data are expressed as means ± SD. 10-HODA 10-hydroxy-12-octadecenoic acid. Source data are provided in the Source Data file.
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Liu, J., Li, H., Tian, Y. et al. Microbial 10-oxostearic acid protects mice against colitis via the nuclear receptor PPARα. Nat Microbiol (2026). https://doi.org/10.1038/s41564-026-02321-7
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DOI: https://doi.org/10.1038/s41564-026-02321-7
