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Lactobacillus rhamnosus GG Protects against Non-Alcoholic Fatty Liver Disease in Mice
Open accessAbstract
OBJECTIVE: Experimental evidence revealed that obesity-associated non-alcoholic fatty liver disease (NAFLD) is linked to changes in intestinal permeability and translocation of bacterial products to the liver. Hitherto, no reliable therapy is available except for weight reduction. Within this study, we examined the possible effect of the probiotic bacterial strain Lactobacillus rhamnosus GG (LGG) as protective agent against experimental NAFLD in a mouse model. METHODS: Experimental NAFLD was induced by a high-fructose diet over eight weeks in C57BL/J6 mice. Fructose was administered via the drinking water containing 30% fructose with or without LGG at a concentration resulting in approximately 5×10(7) colony forming units/g body weight. Mice were examined for changes in small intestinal microbiota, gut barrier function, lipopolysaccharide (LPS) concentrations in the portal vein, liver inflammation and fat accumulation in the liver. RESULTS: LGG increased beneficial bacteria in the distal small intestine. Moreover, LGG reduced duodenal IκB protein levels and restored the duodenal tight junction protein concentration. Portal LPS (P≤0.05) was reduced and tended to attenuate TNF-α, IL-8R and IL-1β mRNA expression in the liver feeding a high-fructose diet supplemented with LGG. Furthermore liver fat accumulation and portal alanine-aminotransferase concentrations (P≤0.05) were attenuated in mice fed the high-fructose diet and LGG. CONCLUSIONS: We show for the first time that LGG protects mice from NAFLD induced by a high-fructose diet. The underlying mechanisms of protection likely involve an increase of beneficial bacteria, restoration of gut barrier function and subsequent attenuation of liver inflammation and steatosis.
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“binge alcohol exposure [232], [233], [234], [235], [236], [237], [238], [239] and nonalcoholic substances including fructose [240], [241], [242] are known to promote gut leakiness, contributing to more severe inflammatory liver disease.”
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“binge alcohol exposure [232], [233], [234], [235], [236], [237], [238], [239] and nonalcoholic substances including fructose [240], [241], [242] are known to promote gut leakiness, contributing to more severe inflammatory liver disease.”
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Metadata
- Authors
- Ritze, Y., Bárdos, G., Claus, A., Ehrmann, V., Bergheim, I., Schwiertz, A., & Bischoff, S. C.
- Affiliations
- University of Hohenheim (DE)
- Institut für Mikroökologie (DE)
- Corresponding author
- Bischoff, Stephan C.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2014-01-27
- Volume
- 9
- Issue
- 1
- Pages
- e80169
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3903470
- OpenAlex
- W2009514456
- Semantic Scholar
- ae2ffaa03bd783feff42333b9541e6a8e65206e6
- Cited by
- 292
- References
- 51
- Citations by year
- 2026: 13 · 2025: 16 · 2024: 28 · 2023: 26 · 2022: 27 · 2021: 23 · 2020: 38 · 2019: 23 · 2018: 19 · 2017: 24 · 2016: 24 · 2015: 20 · 2014: 11
- FWCI
- 37.75
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Danone
- Bundesministerium für Bildung und Forschung (01GI0843, FKZ: 01GI0843)
- Topics
- Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- Lactobacillus rhamnosus GG, non-alcoholic fatty liver disease, probiotics, high-fructose diet, intestinal permeability, intestinal barrier, lipopolysaccharide, gut microbiota, liver inflammation, hepatic steatosis, tight junctions, obesity
- MeSH terms
- Alanine Transaminase, Analysis of Variance, Animals, Dextrans, Fatty Liver, Fructose, Humans, Immunohistochemistry, Intestine, Small, Mice, Inbred C57BL, Permeability, DNA Primers, Caco-2 Cells, Probiotics, Mice, Lacticaseibacillus rhamnosus, Real-Time Polymerase Chain Reaction, Non-alcoholic Fatty Liver Disease
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