ArticleiScience2026
Microbiome-derived metabolites alleviate chronic pain in a reserpine-induced model of fibromyalgia.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Therapeutic and research frontiers in fibromyalgia: integrating pathophysiology with innovative drug repurposing.Inflammopharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibromyalgia is a chronic pain disorder driven by central sensitization and neuroinflammation, increasingly linked to gut-brain axis dysfunction. Here, we delineate a gut-to-CNS axis for pain modulation, demonstrating that an acetate-producing diet alleviates reserpine-induced-fibromyalgia in a rodent model. We show that diet rich in acetylated high-amylose maize starch shifts the gut microbiome to favor acetate-producing bacteria, increasing systemic acetate levels and reducing pain hypersensitivity. This is associated with reduced spinal microglia activation and anti-inflammatory cytokine gene expression, with elevated IL-10 mRNA in the DRG and IL-10, IL-2, and IL-6 in the spinal cord. Electrophysiologically, we observe reduced hyperexcitability in the dorsal horn and increased inhibitory activity. The mechanism driving this change involves reduced prostaglandin-E2 (PGE2)-mediated suppression of glycinergic inhibition, a direct consequence of maintaining microglia in quiescent state. These findings link dietary metabolites to reduced fibromyalgia-like pathology and identify targeted nutrition as a potential disease-modifying therapy for chronic pain.
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.