Total fecal microbiota transplantation alleviates high-fat diet-induced steatohepatitis in mice via beneficial regulation of gut microbiota
Open accessAbstract
Non-alcoholic steatohepatitis (NASH) is an epidemic metabolic disease with limited therapeutic strategies. Cumulative data support the pivotal role of gut microbiota in NASH. Here, we investigated the hypothesis regarding whether fecal microbiota transplantation (FMT) is effective in attenuating high-fat diet (HFD)-induced steatohepatitis in mice. Mice were randomized into control, HFD and HFD + FMT groups. After an 8-week HFD, FMT treatment was initiated and carried out for 8 weeks. The gut microbiota structure, butyrate concentrations of the cecal content, liver pathology and intrahepatic lipid and cytokines were examined. Our results showed that after FMT, the gut microbiota disturbance was corrected in HFD-fed mice with elevated abundances of the beneficial bacteria Christensenellaceae and Lactobacillus . FMT also increased butyrate concentrations of the cecal content and the intestinal tight junction protein ZO-1, resulting in relief of endotoxima in HFD-fed mice. Steatohepatitis was alleviated after FMT, as indicated by a significant decrease in intrahepatic lipid accumulation (reduced Oli-red staining, decreased intrahepatic triglyceride and cholesterol), intrahepatic pro-inflammatory cytokines, and the NAS score. Accordingly, intrahepatic IFN-γ and IL-17 were decreased, but Foxp3, IL-4 and IL-22 were increased after FMT intervention. These data indicate that FMT attenuated HFD-induced steatohepatitis in mice via a beneficial effect on the gut microbiota.
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Fecal microbiota transplantation from healthy mice attenuates steatohepatitis in high-fat-diet-treated mice.
“Conversely, fecal microbiota transplantation from healthy mice attenuated steatohepatitis in high fat diet treated mice 66.”
From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [66]
Transplantation of fecal microbiota from patients with obesity, steatosis or type 2 diabetes can partly reproduce the donor's metabolic phenotype in mouse recipients.
“transplantation of the fecal microbiota from patients with obesity, steatosis or type 2 diabetes can partly reproduce the donor’s metabolic phenotype in mouse recipients [4–7].”
From Dietary lipids, gut microbiota and lipid metabolism (2019) · cites this paper as [5]
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- Authors
- Zhou, D., Pan, Q., Shen, F., Cao, H.-X., Ding, W.-J., Chen, Y.-W., & Fan, J.-G.
- Affiliations
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Fan, Jian-gao
- Venue
- Scientific Reports
- Published
- 2017-05-08
- Volume
- 7
- Issue
- 1
- Pages
- 1529-1529
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5431549
- OpenAlex
- W2611378632
- Cited by
- 421
- References
- 54
- Citations by year
- 2026: 32 · 2025: 59 · 2024: 58 · 2023: 55 · 2022: 57 · 2021: 55 · 2020: 41 · 2019: 33 · 2018: 23 · 2017: 7
- FWCI
- 11.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81470840, 81070322, 81270491, 2012CB517501)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- fecal microbiota transplantation, nonalcoholic steatohepatitis, high-fat diet, gut microbiota, butyrate, Christensenellaceae, Lactobacillus, ZO-1, intestinal tight junctions, endotoxemia, inflammatory cytokines, Foxp3, Th1/Th2 balance, IL-17, interferon-gamma
- MeSH terms
- Gastrointestinal Microbiome, Fecal Microbiota Transplantation, Adipose Tissue, Transaminases, Animals, Body Weight, Cecum, Epididymis, Inflammation, Insulin Resistance, Intestine, Small, Liver, Male, Mice, Inbred C57BL, Obesity, Tight Junctions, Endotoxemia, Butyric Acid, Diet, High-Fat, Non-alcoholic Fatty Liver Disease
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