ArticleThe Journal of biological chemistry2009
Fibroblast growth factor-19, a novel factor that inhibits hepatic fatty acid synthesis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.
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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
109 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.
- Bile Acids and FXR: Novel Targets for Liver Diseases.Frontiers in medicine · 2020Pooled it
- Impact of obeticholic acid on the lipoprotein profile in patients with non-alcoholic steatohepatitis.Journal of hepatology · 2020Trial
- Trial
- The role of FGF19-FGFR4 signaling pathway in liver health and disease: Guardian or destroyer.Genes & diseases · 2026Review
- Tomosyn-2 Regulates Postnatal β-Cell Expansion and Insulin Secretion to Maintain Glucose Homeostasis.Diabetes · 2026Article
- Activation of Brown Adipocytes by Farnesoid X Receptor Agonist, Obeticholic Acid-A Potential Novel Therapeutic Avenue in the Management of Obesity.Journal of clinical medicine · 2026Review
- Integrating bile acid metabolism into precision nutrition strategies for improved swine performance.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Review
- Pan-hypoileism: an endocrine disease.Einstein (Sao Paulo, Brazil) · 2026Review
- Article
- Bile acids and bile acid modification in health and disease: from novel modifications to therapeutic interventions.Frontiers in endocrinology · 2026Review
- The role of gut microbiome disruption in the development of metabolic dysfunction-associated kidney disease.Acta biochimica Polonica · 2026Review
- Proteomic and Demographic Comparisons of Recurrent Ischemic Stroke Patients.Translational stroke research · 2025Article
- Fibroblast growth factor 19-fibroblast growth factor receptor 4 axis: From oncogenesis to targeted-immunotherapy in advanced hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Review
- Secreted proteins in treating metabolic dysfunction-associated steatotic liver disease: from bench towards bedside.Protein & cell · 2025Review
- Host-Microbiome Interaction in the Intensive Care Unit.Diseases (Basel, Switzerland) · 2025Review
- Role of FGF-19, FGF-21 and FGF-23 in Fetal and Neonatal Growth.Journal of clinical medicine · 2025Review
- Pathogenetic therapeutic approaches for endocrine diseases based on antisense oligonucleotides and RNA-interference.Frontiers in endocrinology · 2025Review
- Bile acids and gut microbiota: interactions and impacts on polycystic ovary syndrome.Frontiers in microbiomes · 2025Review
- Bile Acid Signaling in Metabolic and Inflammatory Diseases and Drug Development.Pharmacological reviews · 2024Review
- Bile acid and nonalcoholic steatohepatitis: Molecular insights and therapeutic targets.Journal of advanced research · 2024Review
49 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that administration of fibroblast growth factor-19 (FGF-19) reverses diabetes, hepatic steatosis, hyperlipidemia, and adipose accretion in animal models of obesity. To investigate the mechanism for this effect, we determined whether FGF-19 modulated hepatic fatty acid synthesis, a key process controlling glucose tolerance and triacylglycerol accumulation in liver, blood, and adipose tissue. Incubating primary hepatocyte cultures with recombinant FGF-19 suppressed the ability of insulin to stimulate fatty acid synthesis. This effect was associated with a reduction in the expression of lipogenic enzymes. FGF-19 also suppressed the insulin-induced expression of sterol regulatory element-binding protein-1c (SREBP-1c), a key transcriptional activator of lipogenic genes. FGF-19 inhibition of lipogenic enzyme expression was not mediated by alterations in the activity of the insulin signal transduction pathway or changes in the activity of ERK, p38 MAPK, and AMP-activated protein kinase (AMPK). In contrast, FGF-19 increased the activity of STAT3, an inhibitor of SREBP-1c expression and decreased the expression of peroxisome proliferator-activated receptor-gamma coactivator-1beta (PGC-1beta), an activator of SREBP-1c activity. FGF-19 also increased the expression of small heterodimer partner (SHP), a transcriptional repressor that inhibits lipogenic enzyme expression via a SREBP-1c-independent mechanism. Inhibition of SREBP-1c activity by changes in STAT3 and PGC-1beta activity and inhibition of gene transcription by an elevation in SHP expression can explain the inhibition of lipogenesis caused by FGF-19. In summary, the inhibitory effect of FGF-19 on insulin activation of hepatic fatty acid synthesis constitutes a mechanism that would explain the beneficial effect of FGF-19 on metabolic syndrome.
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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.