Loading
Life sciences · Journal article
The Isme Journal · September 2, 2026
Raises a question worth testing. It does not answer one.
This is a preclinical mechanistic study combining human metagenomic observation with experimental mouse models to establish that microbial hydrogen sulfide suppresses hepatic PPARα signaling and promotes metabolic dysfunction. The work identifies a candidate pathway but remains in mouse models with only observational human data; it does not establish causality or clinical benefit in humans.
Experimental mouse models integrated with human metagenomic analysis and in vitro cellular assays. Mouse models and human clinical cohorts with obesity and glucose metabolism disorders; specific inclusion/exclusion criteria and cohort characteristics not detailed. Intervention: Administration of H2S-producing Desulfovibrio desulfuricans, engineered Escherichia coli expressing phsABC, H2S donor NaHS, PPAR agonist, and H2S adsorbent in mouse models. Compared with: Control groups in mice; specific comparator details not reported in abstract.
Human cohorts with obesity and glucose metabolism disorders showed notable enrichment of genes involved in sulfur transport and H2S production In mouse models, H2S-producing Desulfovibrio desulfuricans, engineered E. coli expressing phsABC, and H2S donor NaHS consistently induced body weight gain and impaired glucose tolerance Transcriptome analysis indicated H2S was associated with downregulation of PPAR signaling pathway and lipid metabolism pathways in liver
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This work identifies a potential microbiome-derived mechanism of metabolic disease but does not provide evidence for clinical intervention. The pathway suppression by PPARα agonists in mice warrants investigation in human trials, but current evidence is preclinical.
Mechanistic mouse model study with human metagenomic association but no human intervention trial; demonstrates pathway mechanism in rodents without clinical outcome data or human causal evidence.
As stated by the source record.
This work identifies a potential microbiome-derived mechanism of metabolic disease but does not provide evidence for clinical intervention. The pathway suppression by PPARα agonists in mice warrants investigation in human trials, but current evidence is preclinical.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
This study investigates the role of gut microbiota-derived hydrogen sulfide (H2S) in obesity and glucose metabolism disorders. By integrating human gut metagenomic data, intervention experiments in mouse models, and in vitro cellular assays, we identified a signature of microbial sulfur metabolism in human cohorts and provided experimental evidence for its causal role and underlying metabolic mechanisms in mice. In clinical cohorts with obesity and glucose metabolism disorders, we observed a notable enrichment of genes involved in sulfur transport and H2S production. In mouse models, administration of H2S-producing Desulfovibrio desulfuricans, engineered Escherichia coli expressing phsABC, and the H2S donor NaHS consistently induced body weight gain and impaired glucose tolerance. Transcriptome analysis and cellular experiments indicated that H2S was associated with downregulation of the PPAR signaling pathway and lipid metabolism pathways in the liver, which may contribute to the abnormal accumulation of lipids and glycogen. Furthermore, rescue experiments using a PPAR agonist and an H2S adsorbent partially reversed these metabolic abnormalities. Collectively, our work provides experimental evidence in mouse models demonstrating that gut microbial H2S promotes metabolic dysfunction through hepatic PPARα suppression, providing potential targets for microbiome-based therapeutic interventions.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.