ArticleNature communications2020
Intestinal FGF15/19 physiologically repress hepatic lipogenesis in the late fed-state by activating SHP and DNMT3A.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 70 citations in OpenAlex.
- Phytosterol-induced modulation of gut microbial bile salt hydrolases ameliorates hyperlipidemia via taurohyodeoxycholic acid-mediated FXR antagonism.Gut microbes · 2026Article
- The role of FGF19-FGFR4 signaling pathway in liver health and disease: Guardian or destroyer.Genes & diseases · 2026Review
- Intestinal FXR agonism synergizes with leptin to improve obesity by reducing appetite via secretin.EMBO reports · 2026Article
- Bioactive Compounds from Edible and Medicinal Mushrooms in Obesity-Depression Comorbidity: Gut-Brain Axis Mechanisms and Functional Food Perspectives.Foods (Basel, Switzerland) · 2026Review
- Mechanism of FXR signaling: from liver inflammation to hepatocellular carcinoma.Biochemistry and biophysics reports · 2026Review
- Evolving Landscape of Systemic Therapy for Hepatocellular Carcinoma: From Targeted Therapy and Combination Strategies to Emerging Therapies.Biomedicines · 2026Review
- DNMT1 facilitates the progression of metabolic dysfunction-associated steatotic liver disease by impeding transcription mediated by HNF4α and PPARα.Clinical and molecular hepatology · 2026Article
- Gestational diabetes as an inter-generational cardiometabolic risk factor: spotlight on emerging exerkines.Cardiovascular diabetology · 2026Review
- Colorectal cancer-derived FGF19 is a metabolically active serum biomarker that exerts enteroendocrine effects on mouse liver.Molecular oncology · 2026Article
- The gut microbiota-bile acid-FXR axis in NAFLD: from progression to therapeutic applications.Frontiers in physiology · 2026Review
- Neutrophils and neutrophil extracellular traps: double-edged swords in cancer pathophysiology and therapy resistance.Cell communication and signaling : CCS · 2025Review
- Orphan Nuclear Receptors in Metabolic Dysfunction-associated Steatotic Liver Disease Development.Journal of clinical and translational hepatology · 2025Review
- Gut-Liver Axis: The Role of Intestinal Microbiota and Their Metabolites in the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.Gut and liver · 2025Review
- Dynamic Rendition of Adipose Genes Under Epigenetic Regulation: Revealing New Mechanisms of Obesity Occurrence.Current issues in molecular biology · 2025Review
- FGF-based drug discovery: advances and challenges.Nature reviews. Drug discovery · 2025Review
- Deficiency of Epithelial PIEZO1 Alleviates Liver Steatosis Induced by High-Fat Diet in Mice.International journal of biological sciences · 2025Article
- Gut microbiota therapy in gastrointestinal diseases.Frontiers in cell and developmental biology · 2025Review
- Folic acid supplementation ameliorates alcohol-induced hepatic steatosis by inhibiting SREBP-1c-mediated lipogenesis.Frontiers in nutrition · 2025Article
- Alterations of DNA methylation profile in peripheral blood of children with simple obesity.Health information science and systems · 2024Article
- Branched-chain amino acids alleviate NAFLD via inhibiting de novo lipogenesis and activating fatty acid β-oxidation in laying hens.Redox biology · 2024Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Hepatic lipogenesis is normally tightly regulated but is aberrantly elevated in obesity. Fibroblast Growth Factor-15/19 (mouse FGF15, human FGF19) are bile acid-induced late fed-state gut hormones that decrease hepatic lipid levels by unclear mechanisms. We show that FGF15/19 and FGF15/19-activated Small Heterodimer Partner (SHP/NR0B2) have a role in transcriptional repression of lipogenesis. Comparative genomic analyses reveal that most of the SHP cistrome, including lipogenic genes repressed by FGF19, have overlapping CpG islands. FGF19 treatment or SHP overexpression in mice inhibits lipogenesis in a DNA methyltransferase-3a (DNMT3A)-dependent manner. FGF19-mediated activation of SHP via phosphorylation recruits DNMT3A to lipogenic genes, leading to epigenetic repression via DNA methylation. In non-alcoholic fatty liver disease (NAFLD) patients and obese mice, occupancy of SHP and DNMT3A and DNA methylation at lipogenic genes are low, with elevated gene expression. In conclusion, FGF15/19 represses hepatic lipogenesis by activating SHP and DNMT3A physiologically, which is likely dysregulated in NAFLD.
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