ArticleThe Journal of biological chemistry2009
Angiopoietin-like 4 (ANGPTL4, fasting-induced adipose factor) is a direct glucocorticoid receptor target and participates in glucocorticoid-regulated triglyceride metabolism.
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. An erratum has been issued. Cited by 92 papers.
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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
92 citing papers in PubMed, 163 citations in OpenAlex.
- Fasting induces ANGPTL4 and reduces LPL activity in human adipose tissue.Molecular metabolism · 2020Trial
- Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct.Diabetes, obesity & metabolism · 2017Trial
- Review
- Hepatic Glucocorticoid Receptor Action and Glucose Homeostasis.Endocrine reviews · 2026Review
- ANGPTL4: A Comprehensive Review of 25 Years of Research.Cancers · 2025Review
- Pemafibrate Induces a Low Level of PPARα Agonist-Stimulated mRNA Expression of ANGPTL4 in ARPE19 Cell.Bioengineering (Basel, Switzerland) · 2024Article
- Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application.Signal transduction and targeted therapy · 2024Review
- Current Challenges and Future Directions in the Assessment of Glucocorticoid Status.Endocrine reviews · 2024Review
- Postprandial exercise regulates tissue-specific triglyceride uptake through angiopoietin-like proteins.JCI insight · 2024Article
- Review
- Characterization of sexual dimorphism in ANGPTL4 levels and function.Journal of lipid research · 2024Article
- Angiopoietin-like protein 4 dysregulation in kidney diseases: a promising biomarker and therapeutic target.Frontiers in pharmacology · 2024Review
- Dual role of ANGPTL4 in inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- ANGPTL4 is a potential driver of HCV-induced peripheral insulin resistance.Scientific reports · 2023Article
- Lipid oxidation dysregulation: an emerging player in the pathophysiology of sepsis.Frontiers in immunology · 2023Review
- α1-Antitrypsin Binds to the Glucocorticoid Receptor with Anti-Inflammatory and Antimycobacterial Significance in Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Profiles of transcriptome and metabolic pathways after hypobaric hypoxia exposure.Proteome science · 2022Article
- Potential of Phage Display Antibody Technology for Cardiovascular Disease Immunotherapy.Journal of cardiovascular translational research · 2022Review
- Intestinal microbiota and their metabolic contribution to type 2 diabetes and obesity.Journal of diabetes and metabolic disorders · 2021Review
- Research Progress on the Involvement of ANGPTL4 and Loss-of-Function Variants in Lipid Metabolism and Coronary Heart Disease: Is the "Prime Time" of ANGPTL4-Targeted Therapy for Coronary Heart Disease Approaching?Cardiovascular drugs and therapy · 2021Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids are important regulators of lipid homeostasis, and chronically elevated glucocorticoid levels induce hypertriglyceridemia, hepatic steatosis, and visceral obesity. The occupied glucocorticoid receptor (GR) is a transcription factor. However, those genes regulating lipid metabolism under GR control are not fully known. Angiopoietin-like 4 (ANGPTL4, fasting-induced adipose factor), a protein inhibitor of lipoprotein lipase, is synthesized and secreted during fasting, when circulating glucocorticoid levels are physiologically increased. We therefore tested whether the ANGPTL4 gene (Angptl4) is transcriptionally controlled by GR. We show that treatment with the synthetic glucocorticoid dexamethasone increased Angptl4 mRNA levels in primary hepatocytes and adipocytes (2-3-fold) and in the livers and white adipose tissue of mice (approximately 4-fold). We tested the mechanism of this increase in H4IIE hepatoma cells and found that dexamethasone treatment increased the transcriptional rate of Angptl4. Using bioinformatics and chromatin immunoprecipitation, we identified a GR binding site within the rat Angptl4 sequence. A reporter plasmid containing this site was markedly activated by dexamethasone, indicative of a functional glucocorticoid response element. Dexamethasone treatment also increased histone H4 acetylation and DNase I accessibility in genomic regions near this site, further supporting that it is a glucocorticoid response element. Glucocorticoids promote the flux of triglycerides from white adipose tissue to liver. We found that mice lacking ANGPTL4 (Angptl4(-/-)) had reductions in dexamethasone-induced hypertriglyceridemia and hepatic steatosis, suggesting that ANGPTL4 is required for this flux. Overall, we establish that ANGPTL4 is a direct GR target that participates in glucocorticoid-regulated triglyceride metabolism.
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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.