ArticleScientific reports2021
Maternal high-fat diet during pregnancy with concurrent phthalate exposure leads to abnormal placentation.
Article in Scientific reports, 2021. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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, 17 citations in OpenAlex.
- Phthalate Exposures and Placental Health in Animal Models and Humans: A Systematic Review.Toxicological sciences : an official journal of the Society of Toxicology · 2022Pooled it
- Bisphenol S fetal exposure in ewes exhibiting contrasted metabolic status impaired the ovarian follicular development of fetuses and lambs.Journal of ovarian research · 2026Article
- Placental toxicity of alternative plasticizers: Current knowledge and future directions.Reproductive toxicology (Elmsford, N.Y.) · 2026Review
- Exposure to phthalates enhances estrogen and beta-catenin signaling pathways, leading to endometrial hyperplasia in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Association of PFAS and Metals with Cardiovascular Disease Risk: Exploring the Mediating Effect of Diet.Environments (Basel, Switzerland) · 2025Article
- Phthalates Impair Estrogenic Regulation of HIF2α and Extracellular Vesicle Secretion by Human Endometrial Stromal Cells.Endocrinology · 2025Article
- Maternal Supplementation withDiseases (Basel, Switzerland) · 2024Article
- Metabolic status is a key factor influencing proteomic changes in ewe granulosa cells induced by chronic BPS exposure.BMC genomics · 2024Article
- Prenatal exposure to Di(2-ethylhexyl) phthalate and high-fat diet synergistically disrupts gonadal function in male mice†.Biology of reproduction · 2024Article
- Chronic exposure of mice to phthalates enhances TGF beta signaling and promotes uterine fibrosis.Reproductive toxicology (Elmsford, N.Y.) · 2023Article
- Exposure to di-isononyl phthalate during early pregnancy disrupts decidual angiogenesis and placental development in mice.Reproductive toxicology (Elmsford, N.Y.) · 2023Article
- Maternal exposure to CeOJournal of nanobiotechnology · 2022Article
- Bisphenol S Alters the Steroidome in the Preovulatory Follicle, Oviduct Fluid and Plasma in Ewes With Contrasted Metabolic Status.Frontiers in endocrinology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Di(2-ethylhexyl) phthalate (DEHP) is a synthetic chemical commonly used for its plasticizing capabilities. Because of the extensive production and use of DEHP, humans are exposed to this chemical daily. Diet is a significant exposure pathway and fatty food contain the highest level of phthalates. The impact on pregnancy following DEHP exposure and the associated interaction of high fat (HF) diet remains unknown. Here we report that exposure of pregnant mice to an environmentally relevant level of DEHP did not affect pregnancy. In contrast, mice fed a HF diet during gestation and exposed to the same level of DEHP display marked impairment in placental development, resulting in poor pregnancy outcomes. Our study further reveals that DEHP exposure combined with a HF diet interfere with the signaling pathway controlled by nuclear receptor PPARγ to adversely affect differentiation of trophoblast cells, leading to compromised vascularization and glucose transport in the placenta. Collectively, these findings demonstrate that maternal diet during pregnancy is a critical factor that determines whether exposure to an environmental toxicant results in impaired placental and fetal development, causing intrauterine growth restriction, fetal morbidity, and mortality.
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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.