ArticleAmerican journal of physiology. Cell physiology2020
Bisphenol AF promotes inflammation in human white adipocytes.
Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- A systematic review of exposure to endocrine disruptors and energy expenditure in mice.Environmental health : a global access science source · 2025Pooled it
- Article
- A Review of the Literature on the Endocrine Disruptor Activity Testing of Bisphenols inJournal of xenobiotics · 2026Review
- Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease.Molecular and cellular biochemistry · 2025Review
- UPLC-QqQMS based targeted metabolomics reveal combination impact on metabolism caused by bisphenol AF and fructose combined exposure in male mice.Scientific reports · 2025Article
- Adipose tissue dysfunction disrupts metabolic homeostasis: mechanisms linking fat dysregulation to disease.Frontiers in endocrinology · 2025Review
- Chronic BPAF exposure differentially enhances fat deposition in mice fed normal or high-fat diets via lipid metabolism dysregulation.Frontiers in endocrinology · 2025Article
- Bisphenol A and Its Emergent Substitutes: State of the Art of the Impact of These Plasticizers on Oxidative Stress and Its Role in Vascular Dysfunction.Antioxidants (Basel, Switzerland) · 2024Review
- Bisphenol A substitutes and obesity: a review of the epidemiology and pathophysiology.Frontiers in endocrinology · 2023Review
- The Combined Partial Knockdown ofAntioxidants (Basel, Switzerland) · 2022Article
- Chemical Exposures Affect Innate Immune Response to SARS-CoV-2.International journal of molecular sciences · 2021Article
- BPA, BPAF and TMBPF Alter Adipogenesis and Fat Accumulation in Human Mesenchymal Stem Cells, with Implications for Obesity.International journal of molecular sciences · 2021Article
- Mitochondrial Epigenetics and Environmental Health: Making a Case for Endocrine Disrupting Chemicals.Toxicological sciences : an official journal of the Society of Toxicology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Endocrine-disrupting chemicals interact with transcription factors essential for adipocyte differentiation. Exposure to endocrine-disrupting chemicals corresponds with elevated risks of obesity, but the effects of these compounds on human cells remain largely undefined. Widespread use of bisphenol AF (BPAF) as a bisphenol A (BPA) alternative in the plastics industry presents unknown health risks. To this end, we discovered that BPAF interferes with the metabolic function of mature human adipocytes. Although 4-day exposures to BPAF accelerated adipocyte differentiation, we observed no effect on mature fat cell marker genes. Additional gene and protein expression analysis showed that BPAF treatment during human adipocyte differentiation failed to suppress the proinflammatory transcription factor STAT1. Microscopy and respirometry experiments demonstrated that BPAF impaired mitochondrial function and structure. To test the hypothesis that BPAF fosters vulnerabilities to STAT1 activation, we treated mature adipocytes previously exposed to BPAF with interferon-γ (IFNγ). BPAF increased IFNγ activation of STAT1 and exposed mitochondrial vulnerabilities that disrupt adipocyte lipid and carbohydrate metabolism. Collectively, our data establish that BPAF activates inflammatory signaling pathways that degrade metabolic activity in human adipocytes. These findings suggest how the BPA alternative BPAF contributes to metabolic changes that correspond with obesity.
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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.