ArticleJournal of endocrinological investigation2026
Chronic low-dose of BPS and PFOS alter adipogenic programming and impair insulin responsiveness in human adipocytes.
Article in Journal of endocrinological investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimobesity is a major global health concern tightly linked to insulin resistance and type 2 diabetes. Environmental exposure to endocrine-disrupting chemicals (EDs), including bisphenols (BPs) and perfluoroalkyl substances (PFs), has been implicated in metabolic dysfunction, yet the impact of chronic low-dose co-exposure on human adipocyte development and insulin responsiveness remains poorly defined. Here, we evaluated bisphenol S (BPS) and perfluorooctane sulfonate (PFOS), alone or combined, in human adipose-derived stem cells undergoing adipogenic differentiation.
methodsCells were chronically exposed to environmentally relevant low doses of bisphenol S (BPS) and perfluorooctane sulfonate (PFOS), alone or in combination, throughout adipogenic differentiation.
resultsLipid droplet accumulation was unchanged across conditions, indicating preserved terminal differentiation. In contrast, BPS and PFOS altered the timing and magnitude of key adipogenic transcriptional programs (CEBPA, PPARγ) and the mature adipocyte marker FABP4. PFOS and BPS+PFOS selectively increased IL1β expression in mature adipocytes, suggesting a limited pro-inflammatory shift. Functionally, all ED-treated groups showed reduced insulin-stimulated glucose uptake, associated with impaired GLUT4 translocation to the plasma membrane despite unchanged total GLUT4 levels. Notably, combined exposure produced the strongest defects in insulin signalling, reducing PI3K pathway activation and decreasing total AKT and ERK1/2 protein levels. In contrast, individually administered BPS and PFOS impaired glucose uptake without detectable PI3K alterations, suggesting the involvement of additional mechanisms.
conclusionOverall, chronic low-dose exposure to BPS and PFOS disrupts adipocyte transcriptional and signalling networks, inducing features consistent with impaired insulin responsiveness and underscoring the importance of considering ED mixtures in metabolic risk assessment.
Indexed as
Identifiers
42645757What Socratic holds
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.