ArticleEuropean journal of nutrition2026
Butyrate ameliorates maternal high-fat-diet-induced placental inflammation and offspring metabolic dysfunction via modulating gut microbiota in mice.
Article in European journal of nutrition, 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
7 authors.
Funding
Abstract
backgroundMaternal high-fat diet (HFD) increases the risk of metabolic disorders in offspring. Placental inflammation acts as a critical mediator with poorly addressed etiology. Recently HFD-induced gut dysbiosis is demonstrated to be a key driver of systemic inflammation. Whether inflammatory signals triggered by HFD-induced gut dysbiosis are transmitted to the placenta via the maternal-fetal axis warrant further investigation. This study aims to elucidate the mechanistic connection between maternal gut dysbiosis and placental inflammation, thereby offering insights into microbiota-mediated developmental origins of metabolic diseases in offspring.
methodsFemale C57BL/6 mice were exposed to high fat diet (HFD) for 5 weeks prior to mating with male mice. Gut microbiota was profiled by using 16 S rRNA sequencing and fecal short-chain fatty acids (SCFAs) were quantified by GC-MS from HFD pregnant mice at gestational day 18.5 (G18.5). Mice were sacrificed at G18.5, and placenta histopathological analysis as well as inflammatory markers and lipopolysaccharide (LPS) level were analyzed. Anti-inflammatory effects of butyrate were evaluated in vitro by using HTR-8/Svneo cells and in vivo through gestational supplementation (0.3 mg/g body weight) in HFD-fed dams.
resultsMaternal HFD exposure induced significant placental inflammation as well as hepatic steatosis in the offspring. HFD-fed dams exhibited distinct gut dysbiosis with reduced fecal and serum SCFAs, which was accompanied by elevated placental LPS levels and exacerbated inflammatory responses. Butyrate treatment suppressed the expression of inflammatory cytokines in vitro through down-regulating the phosphorylation of NF-κB, ERK1/2 signaling pathways via G-protein-coupled receptor 41 (GPR41). Furthermore, gestational butyrate intervention effectively alleviated placental inflammation and mitigated fetal hepatic lipid deposition in HFD-exposed offspring.
conclusionPlacental inflammation caused by maternal HFD is closely associated with gut microbiota dysbiosis. Butyrate supplementation during gestation reduces placental inflammation and ameliorated offspring hepatic steatosis, highlighting the therapeutic potential of butyrate for mitigating the adverse metabolic programming effects upon maternal HFD exposure.
Indexed as
Identifiers
42377574What OpenQuestion 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 OpenQuestion graph.