ArticleEnvironment & health (Washington, D.C.)2026
Inulin Mitigates Reproductive Toxicity from Early Life GenX Exposure in Mice by Inhibiting LPS-TLR4-Mediated Necroptosis: Exploring the Gut-Testis Axis.
Article in Environment & health (Washington, D.C.), 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hexafluoropropylene oxide dimer acid (HFPO-DA or GenX), a common short-chain substitute for perfluorooctanoic acid, affects mammalian development. However, the effects of GenX on male reproductive development remain incompletely understood. In this study, pregnant mice were administered GenX (2 mg/kg bw/d) via gavage and/or inulin (1% w/v) in the drinking water until lactation concluded. At the 16th week after birth, male littermates were necropsied. Early-life exposure to GenX in mice led to gut microbiota imbalance, colonic tissue alterations, reduced expression of goblet cells and tight junction proteins (ZO-1, occludin, and claudin 5), and triggered an inflammatory response. Moreover, increased serum LPS levels, histopathological alterations in testicular tissue, reduced testosterone levels, and decreased expression of blood-testis barrier proteins (ZO-1, occludin, N-cadherin, and β-catenin) were resulted from early-life exposure to GenX. Additionally, there was an upregulation of inflammatory factors TNF-a and IL-1β, along with a higher incidence of sperm abnormalities. Transcriptomic analysis revealed an enrichment of necroptosis in the testes of the GenX group. Consistently, overexpression of RIPK1, RIPK3, TLR4, and p-ERK, and decreased expression of caspase-8 confirmed the participation of necroptosis in GenX-induced testicular injury. As a potent prebiotic, inulin balanced intestinal homeostasis and attenuated GenX-induced testicular injury by modulating LPS-TLR4-mediated necroptosis. This study offers new insights into the impact of early-life GenX exposure on male reproductive risk and evaluates the potential of inulin as a dietary modification strategy.
Indexed as
Identifiers
What 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.