ArticleFrontiers in microbiology2026
Gut microbiota dysbiosis aggravates liver injury in acute-on-chronic liver failure through D-lactate accumulation.
Article in Frontiers in microbiology, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Acute-on-chronic liver failure (ACLF) is a life-threatening condition arising from the abrupt worsening of pre-existing chronic liver disease, typically accompanied by multi-organ failure and markedly elevated short-term mortality. Gut microbiota dysbiosis is frequently observed in patients with ACLF, yet the mechanisms by which microbial alterations contribute to disease progression remain unclear. Here, we investigated whether gut microbiota dysbiosis could exacerbate liver injury in ACLF and explored the underlying mechanisms. Methods: The correlation between serum lactic acid levels and liver injury in patients with ACLF was analyzed. ACLF model in SD rats was established to investigate the effects of lactate transporter inhibitor on liver injury. 16S rRNA sequencing was performed to characterize alterations in the gut microbiota of ACLF rats, and correlations between serum lactate levels, fecal lactate levels and liver injury-related indicators were evaluated. A pseudo-germ-free ACLF rat model was established to determine whether gut microbiota dysbiosis could aggravate liver injury in ACLF rats. Results: Serum L-lactate and D-lactate levels were significantly positively correlated with ALT levels in patients with ACLF. Moreover, inhibiting lactic acid transport exacerbated liver injury in ACLF rats. The abundance of lactate-producing bacteria, particularly Conclusion: Our results suggested that gut microbiota dysbiosis may contribute to ACLF progression, potentially through expansion of lactate-producing bacteria and subsequent D-lactic acid accumulation. Our results provided a conceptual basis for targeting microbial lactic acid metabolism as a therapeutic strategy for ACLF.
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.