ArticleProceedings of the National Academy of Sciences of the United States of America2016
Forkhead box A3 mediates glucocorticoid receptor function in adipose tissue.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
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- Adipocyte CLDN5 promotes thermogenesis and energy expenditure through regulation of IL10 expression.Nature communications · 2025Article
- FOXA3 regulates cholesterol metabolism to compensate for low uptake during the progression of lung adenocarcinoma.PLoS biology · 2024Article
- Glucocorticoids increase adiposity by stimulating Krüppel-like factor 9 expression in macrophages.Nature communications · 2024Article
- Characterisation of forkhead box protein A3 as a key transcription factor for hepatocyte regeneration.JHEP reports : innovation in hepatology · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Fresh insights into glucocorticoid-induced diabetes mellitus and new therapeutic directions.Nature reviews. Endocrinology · 2022Review
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- BNIP3L/NIX-mediated mitophagy protects against glucocorticoid-induced synapse defects.Nature communications · 2021Article
- Molecular Mechanisms of Glucocorticoid-Induced Insulin Resistance.International journal of molecular sciences · 2021Review
- Autophagy inhibition prevents glucocorticoid-increased adiposity via suppressing BAT whitening.Autophagy · 2020Article
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- Hepatic Forkhead Box Protein A3 Regulates ApoA-I (Apolipoprotein A-I) Expression, Cholesterol Efflux, and Atherogenesis.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Ablation of PPARγ in subcutaneous fat exacerbates age-associated obesity and metabolic decline.Aging cell · 2018Article
- Glucocorticoid Receptor and Adipocyte Biology.Nuclear receptor research · 2018Article
- Treatment of Diabetic Mice with a Combination of Ketogenic Diet and Aerobic Exercise via Modulations of PPARs Gene Programs.PPAR research · 2018Article
- Adipocyte glucocorticoid receptor is important in lipolysis and insulin resistance due to exogenous steroids, but not insulin resistance caused by high fat feeding.Molecular metabolism · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Glucocorticoids (GCs) are widely prescribed anti-inflammatory agents, but their chronic use leads to undesirable side effects such as excessive expansion of adipose tissue. We have recently shown that the forkhead box protein A3 (Foxa3) is a calorie-hoarding factor that regulates the selective enlargement of epididymal fat depots and suppresses energy expenditure in a nutritional- and age-dependent manner. It has been demonstrated that Foxa3 levels are elevated in adipose depots in response to high-fat diet regimens and during the aging process; however no studies to date have elucidated the mechanisms that control Foxa3's expression in fat. Given the established effects of GCs in increasing visceral adiposity and in reducing thermogenesis, we assessed the existence of a possible link between GCs and Foxa3. Computational prediction analysis combined with molecular studies revealed that Foxa3 is regulated by the glucocorticoid receptor (GR) in preadipocytes, adipocytes, and adipose tissues and is required to facilitate the binding of the GR to its target gene promoters in fat depots. Analysis of the long-term effects of dexamethasone treatment in mice revealed that Foxa3 ablation protects mice specifically against fat accretion but not against other pathological side effects elicited by this synthetic GC in tissues such as liver, muscle, and spleen. In conclusion our studies provide the first demonstration, to our knowledge, that Foxa3 is a direct target of GC action in adipose tissues and point to a role of Foxa3 as a mediator of the side effects induced in fat tissues by chronic treatment with synthetic steroids.
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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.