ArticleGut microbes2023
Disruption of the microbiota-gut-brain axis is a defining characteristic of the α-Gal A (-/0) mouse model of Fabry disease.
Article in Gut microbes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
- A Combined Colon Organoid-Sensory Neuron Model Reveals Epithelial Contribution to Moringin Efficacy Against Painful Inflammatory Bowel Disease.Phytotherapy research : PTR · 2026Article
- Article
- Gut-Brain Axis Dysregulation in Inflammatory Bowel Disease: Implications for Coagulation Abnormalities and Extraintestinal Manifestations.International journal of general medicine · 2026Review
- Article
- Intestinal inflammation induces glymphatic remodeling, priming early neurodegenerative signals in male mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Review
- Benefits ofInternational journal of molecular sciences · 2025Article
- Role of microbiota in pain: From bench to bedside.iMetaOmics · 2025Review
- Hydrogen Sulfide (HNeurochemical research · 2025Article
- Gut-Heart Axis: Microbiome Involvement in Restrictive Cardiomyopathies.Biomedicines · 2025Review
- Systemic metabolic reprogramming and microbial dysbiosis in Fabry disease: Multi-omics mechanisms and implications for drug development.Frontiers in pharmacology · 2025Review
- Diabetic Neuropathic Pain: Directions for Exploring Treatments.Biomedicines · 2024Review
- Mechanistic Intimate Insights into the Role of Hydrogen Sulfide in Alzheimer's Disease: A Recent Systematic Review.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fabry disease (FD) is an X-linked metabolic disease caused by a deficiency in α-galactosidase A (α-Gal A) activity. This causes accumulation of glycosphingolipids, especially globotriaosylceramide (Gb3), in different cells and organs. Neuropathic pain and gastrointestinal (GI) symptoms, such as abdominal pain, nausea, diarrhea, constipation, and early satiety, are the most frequent symptoms reported by FD patients and severely affect their quality of life. It is generally accepted that Gb3 and lyso-Gb3 are involved in the symptoms; nevertheless, the origin of these symptoms is complex and multifactorial, and the exact mechanisms of pathogenesis are still poorly understood. Here, we used a murine model of FD, the male α-Gal A (-/0) mouse, to characterize functionality, behavior, and microbiota in an attempt to elucidate the microbiota-gut-brain axis at three different ages. We provided evidence of a diarrhea-like phenotype and visceral hypersensitivity in our FD model together with reduced locomotor activity and anxiety-like behavior. We also showed for the first time that symptomology was associated with early compositional and functional dysbiosis of the gut microbiota, paralleled by alterations in fecal short-chain fatty acid levels, which partly persisted with advancing age. Interestingly, most of the dysbiotic features suggested a disruption of gut homeostasis, possibly contributing to accelerated intestinal transit, visceral hypersensitivity, and impaired communication along the gut-brain axis.
Indexed as
Identifiers
What 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.