ArticleCell reports2021
High-fat diet-activated fatty acid oxidation mediates intestinal stemness and tumorigenicity.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 2 of them syntheses 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.
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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
126 citing papers in PubMed, 2 syntheses or guidelines pooled it, 191 citations in OpenAlex.
- Interplay of chronic obstructive pulmonary disease and colorectal cancer development: unravelling the mediating role of fatty acids through a comprehensive multi-omics analysis.Journal of translational medicine · 2023Pooled it
- Effect of Ketogenic Diets on Body Composition and Metabolic Parameters of Cancer Patients: A Systematic Review and Meta-Analysis.Nutrients · 2022Pooled it
- Gut microbiota and immunometabolism in obesity.Gut microbes · 2026Review
- Compartment-specific PPARδ activity controls the outcome of cancer-immune cell competition and immunotherapy efficacy.Nature immunology · 2026Article
- Regional organization of nutrient absorption across the small intestine.Nature reviews. Gastroenterology & hepatology · 2026Review
- Diet-Induced Phospholipid Remodeling Dictates Ferroptosis Sensitivity and Tumorigenesis in the Pancreas.Cancer discovery · 2026Article
- ALDH1B1 promotes mitochondrial γ-butyrobetaine biosynthesis and fatty acid oxidation in colorectal cancer.bioRxiv : the preprint server for biology · 2026Article
- Immune checkpoints and immunoregulation in metabolic diseases and cancers: pathological mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2026Review
- Dietary Regulation of Intestinal Stem Cell Function: Nutrient-Sensing, Microbiota-Mediated, and Regenerative Mechanisms from a Dietetic Perspective.Biomedicines · 2026Review
- Molecular basis of HACD-TECR complex mediated very-long-chain fatty acid elongation reveal a potential target in colorectal cancer.Science advances · 2026Article
- Chrono-atlas of cell-type specific daily gene expression rhythms in the regenerating colon.Nature communications · 2026Article
- Lineage plasticity driven by GATA6 loss fuels colorectal cancer metastasis.Cell stem cell · 2026Article
- PPARα activation overcomes fibroinflammatory liver microenvironment-associated anti-PD-1 resistance in hepatocellular carcinoma by mediating GSDME-dependent pyroptosis.Nature communications · 2026Article
- Stem cells as an essential mediator of the exercise-tumorigenesis link.Nature reviews. Cancer · 2026Review
- Article
- Lipidomic profiling reveals age-dependent changes in plasma membrane lipids that affect neural stem cell aging.Science advances · 2026Article
- Fatty Acid Metabolism and Hypoxia in the Tumor Microenvironment: Metabolic Adaptation and Clinical Potential in Colorectal Cancer.Biomedicines · 2026Review
- Celastrol at the obesity-cancer interface: critical appraisal of molecular mechanisms, preclinical evidence, and translational barriers.Molecular biology reports · 2026Review
- Article
- Cannabidiol triggers fatty acids β-oxidation mediated by Stat2 to facilitate intestinal stem cells regeneration post radiation.Experimental & molecular medicine · 2026Article
66 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 7 institutions in 4 countries.
Funding
Abstract
Obesity is an established risk factor for cancer in many tissues. In the mammalian intestine, a pro-obesity high-fat diet (HFD) promotes regeneration and tumorigenesis by enhancing intestinal stem cell (ISC) numbers, proliferation, and function. Although PPAR (peroxisome proliferator-activated receptor) nuclear receptor activity has been proposed to facilitate these effects, their exact role is unclear. Here we find that, in loss-of-function in vivo models, PPARα and PPARδ contribute to the HFD response in ISCs. Mechanistically, both PPARs do so by robustly inducing a downstream fatty acid oxidation (FAO) metabolic program. Pharmacologic and genetic disruption of CPT1A (the rate-controlling enzyme of mitochondrial FAO) blunts the HFD phenotype in ISCs. Furthermore, inhibition of CPT1A dampens the pro-tumorigenic consequences of a HFD on early tumor incidence and progression. These findings demonstrate that inhibition of a HFD-activated FAO program creates a therapeutic opportunity to counter the effects of a HFD on ISCs and intestinal tumorigenesis.
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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.