Shock (Augusta, Ga.)
June 11, 2026 · via Europe PMC
Gut Microbiota Modulation Attenuates Myocardial Ischemia-Reperfusion Injury in Diabetic Mice.
Takahashi K, Yoshikawa Y, Chaki T, Yamakage M.
AI summary — for doctors, generated from the abstract only
In diabetic mice, transplanting gut microbiota from non-diabetic donor mice reduced the size of heart damage after induced myocardial ischemia-reperfusion injury, associated with partial changes in gut microbial composition.
What was studied
A preclinical study in male diabetic (db/db) mice receiving a 14-day course of fecal microbiota transplantation (FMT) from lean non-diabetic donor mice versus vehicle, followed by induced myocardial ischemia-reperfusion injury (IRI), with infarct size and gut microbiota composition (16S rRNA sequencing) as outcomes.
Key findings
- FMT significantly reduced infarct size as a percentage of area at risk compared with the IRI-only group (38.7% ± 13.4% vs 58.7% ± 4.3%, P = 0.003).
- Diabetic mice showed distinct gut microbial community structure from donor mice, with the microbiome intervention producing a modest but significant shift in community composition.
- Akkermansia muciniphila was identified as a candidate bacterial taxon that was reduced in diabetic mice and partially restored after FMT.
Clinical relevance
This is a preclinical mouse study and does not demonstrate a treatment effect in diabetic patients; it suggests gut microbiota composition as a potential contributor to diabetic heart vulnerability to ischemia-reperfusion injury, which could inform future translational research but has no current clinical application.
Who should care
Limitations
All experiments were conducted in a mouse model of type 2 diabetes, so findings may not translate to human patients; the abstract does not report whether the infarct-size reduction translated into functional cardiac outcomes or long-term survival.
Gut microbiota transplantation reduced heart injury after induced ischemia-reperfusion in diabetic mice, an early preclinical finding.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Background
The gut microbiome is increasingly being recognized as a regulator of cardiometabolic health; however, whether the microbiome interventions can attenuate myocardial ischemia-reperfusion injury (IRI) in diabetic hearts remains unclear. Therefore, we tested whether fecal microbiota transplantation (FMT) from lean nondiabetic donors could mitigate myocardial IRI in type 2 diabetes mellitus db/db mice and explored candidate taxa associated with protection.
Methods
Male db/db mice (type 2 diabetes mellitus model) received a 14-day course of FMT from lean db/m donors or a vehicle after antibiotic pretreatment. Myocardial IRI was induced, and infarct size was quantified. The gut microbiota was evaluated by 16S rRNA gene sequencing.
Results
FMT significantly reduced the infarct size as a percentage of the area at risk compared to the IRI group (38.7 ± 13.4% vs. 58.7 ± 4.3%, P = 0.003). Microbiome analysis revealed that among alpha-diversity metrics, only the Simpson index differed between the donor and diabetic groups. In beta-diversity analyses, diabetic mice clustered separately from donor mice, and the microbiome intervention induced a modest but significant shift detected by the presence or absence of Unweighted UniFrac. Differential abundance analysis and exploratory linear discriminant analysis effect size further suggested Akkermansia , particularly A. muciniphila , as a candidate taxon reduced in diabetic mice and partially restored after the FMT intervention.
Conclusion
A donor-derived microbiome intervention attenuated myocardial IRI in db/db mice and was accompanied by partial remodeling of the gut microbiota. A. muciniphila emerged as a candidate taxon associated with a reduced susceptibility to IRI in diabetic hearts.
DOI
10.1097/shk.0000000000002882
PMID
42275128
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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