ArticleToxicology and applied pharmacology2020
Perfluorooctanesulfonic acid (PFOS) administration shifts the hepatic proteome and augments dietary outcomes related to hepatic steatosis in mice.
Article in Toxicology and applied pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 3 of them syntheses 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.
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Who cites it
31 citing papers in PubMed, 3 syntheses or guidelines pooled it, 52 citations in OpenAlex.
- Exposure to Per- and Polyfluoroalkyl Substances and Liver Cancer: A Systematic Review of Animal and Epidemiological Studies.Environmental science & technology · 2026Pooled it
- Studying the Impact of Persistent Organic Pollutants Exposure on Human Health by Proteomic Analysis: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Exposure to per- and Polyfluoroalkyl Substances and Markers of Liver Injury: A Systematic Review and Meta-Analysis.Environmental health perspectives · 2022Pooled it
- Presence of Legacy and Emerging PFAS in Human Liver Specimens Banked in the United States from 2000 to 2024.Environmental science & technology · 2026Article
- Identification of functional genetic components modulating toxicity response to PFOS using genome-wide CRISPR screens in HepG2/C3A cells.Archives of toxicology · 2026Article
- Impact of PFAS exposure on lipid metabolic pathways: mechanisms and implicatins in carcinogenesis.Frontiers in toxicology · 2026Review
- Identification of Functional Genetic Components Modulating Toxicity Response to PFOS using Genome-wide CRISPR Screens in HepG2/C3A cells.bioRxiv : the preprint server for biology · 2025Article
- Review
- Systemic chronic inflammation mediates the effect of per- and polyfluoroalkyl substances exposure on the risk of nonalcoholic fatty liver disease: A cross-sectional study among Chinese government employees.Environmental epidemiology (Philadelphia, Pa.) · 2025Article
- Perfluorooctane sulfonate exposure and alcohol-associated liver disease severity in a mouse chronic-binge ethanol feeding model.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Single-cell RNA sequencing reveals tissue-specific transcriptomic changes induced by perfluorooctanesulfonic acid (PFOS) in larval zebrafish (Danio rerio).Journal of hazardous materials · 2025Article
- Dose-response modeling of effects in mice after exposure to a polyfluoroalkyl substance (Nafion byproduct 2).Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Effects of Perfluorooctane Sulfonic Acid Exposure on Intestinal Microbial Community, Lipid Metabolism, and Liver Lesions in Mice.International journal of molecular sciences · 2025Article
- Effects of PFAS on human liver transporters: implications for health outcomes.Toxicological sciences : an official journal of the Society of Toxicology · 2024Review
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- Sex, Nutrition, and NAFLD: Relevance of Environmental Pollution.Nutrients · 2023Review
- Article
- A review of cardiovascular effects and underlying mechanisms of legacy and emerging per- and polyfluoroalkyl substances (PFAS).Archives of toxicology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatic steatosis increases risk of fatty liver and cardiovascular disease. Perfluorooctanesulfonic acid (PFOS) is a persistent, bio-accumulative pollutant that has been used in industrial and commercial applications. PFOS administration induces hepatic steatosis in rodents and increases lipogenic gene expression signatures in cultured hepatocytes. We hypothesized that PFOS treatment interferes with lipid loss when switching from a high fat diet (HFD) to a standard diet (SD), and augments HFD-induced hepatic steatosis. Male C57BL/6 N mice were fed standard chow diet or 60% kCal high-fat diet (HFD) for 4 weeks to increase body weight. Then, some HFD mice were switched to SD and mice were further divided to diet only or diet containing 0.0003% PFOS, for six treatment groups: SD, HFD to SD (H-SD), HFD, SD + PFOS, H-SD + PFOS, or HFD + PFOS. After 10 weeks on study, blood and livers were collected. HFD for 14 weeks increased body weight and hepatic steatosis, whereas H-SD mice returned to SD measures. PFOS administration reduced body weight in mice fed a SD, but not H-SD or HFD. PFOS administration increased liver weight in H-SD + PFOS and HFD + PFOS mice. PFOS increased hepatic steatosis in H-SD and HFD groups. Hepatic mRNA expression and SWATH-MS proteomic analysis revealed that PFOS induced lipid and xenobiotic transporters, as well as metabolism pathways. Overall, the findings herein suggest that PFOS treatment did interfere with lipid loss associated with switch to a SD and similarly augmented hepatic lipid accumulation in mice established on an HFD.
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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 Socratic graph.