ArticleNutrition & metabolism2026
Exploring gut microbiota mechanisms in frailty induced by 5-hydroxymethylfurfural: evidence from mouse models and Mendelian randomization.
Article in Nutrition & metabolism, 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
11 authors.
Funding
Abstract
Frailty in older adults has been linked to gut microbiota, but the underlying mechanisms remain unclear. This study investigates the relationship between gut microbiota and frailty, focusing on the potential mediating roles of serum metabolites, immune cells, and inflammatory proteins. We used a combination of mouse model experiments and Mendelian randomization (MR) analysis to examine how gut microbiota contributes to frailty development. In a mouse model of chronic inflammation-induced frailty, a standardized frailty index was used for assessment. High-throughput 16 S rRNA sequencing revealed significant gut microbiota dysbiosis in frail mice, with a notable elevation in Ruminococcus abundance. Spearman correlation analysis showed a strong positive association between Ruminococcus, frailty scores (⍴ = 0.716, P < 0.001), and inflammatory markers. Metabolomic profiling further identified key metabolites linked to frailty, including S-Methyl-5’-thioadenosine, L-anserine, and indolelactic acid (IAA), with IAA showing a significant correlation with Ruminococcus (P < 0.001). To validate these findings, MR analysis was performed using data from the European Bioinformatics Institute and the MiBioGen consortium. The analysis confirmed a causal relationship between Ruminococcus and frailty (OR = 1.035, 95% CI: 1.011–1.059, P = 0.004). Additionally, HLA-DR expression on CD14 + monocytes was identified as a partial mediator of the effect of Ruminococcus obeum on frailty. Importance. • Chronic-inflammation model establishes frailty in mice, quantified via a validated frailty index. • Gut dysbiosis characteristic of frailty, notably a elevation in Ruminococcus. • Strong link between Ruminococcus and frailty/inflammation, with Spearman’s ⍴ = 0.716. • Serum metabolites (S-MTA, L-anserine, IAA) correlate with frailty—IAA particularly tracks with Ruminococcus levels. • Mendelian randomization confirms causality: genetically higher Ruminococcus increases frailty risk. • CD14⁺ monocyte HLA-DR expression partially mediates the effect of Ruminococcus obeum on frailty.
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.