ArticleNature communications2026
Sialic acid exacerbates polycystic ovary syndrome in mice by modulating gut microbiota-mediated bile acid metabolism and FXR activation.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Gut microbiota in PCOS: key microbial changes, potential mechanisms and clinical applications.Journal of translational medicine · 2026Review
- Decoding the gut-adipose-ovary axis in polycystic ovary syndrome: from metabolic dysregulation to oncological risk modulation.Frontiers in microbiology · 2026Review
- A novel strategy for controlled release of sialic acid based on W1/O/W2 emulsion microencapsulation for gut microbiota modulation.Current research in food science · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women. Accumulating evidence indicates that gut dysbiosis and metabolic disturbances are associated with the pathogenesis of PCOS. However, the mechanisms by which metabolic alterations influence gut homeostasis and contribute to PCOS progression remain poorly understood. Here, we show that N-acetylneuraminic acid (Neu5Ac) exacerbates dehydroepiandrosterone (DHEA)-induced PCOS phenotypes in female mice in a gut microbiota-dependent manner. Specifically, Neu5Ac promotes the expansion of the gut Ligilactobacillus salivarius (L. sa) with bile salt hydrolase (BSH) activity. Administration of L. sa to DHEA-treated mice worsens PCOS symptoms by reducing levels of the conjugated bile acid tauroursodeoxycholic acid (TUDCA) via BSH activity. Reduced TUDCA enhances intestinal farnesoid X receptor (FXR) activation, leading to suppression of IL-22 production. Mechanistically, IL-22 attenuates DHEA-induced ovarian ferroptosis by activating the STAT3 signaling pathway. These findings reveal that sialic acid-mediated bile acid-FXR-IL-22 signaling contributes to PCOS pathogenesis, highlighting a potential therapeutic strategy for PCOS intervention.
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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.