Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.

<h4>Objective</h4>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....

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Autores principales: Yvonne Ritze, Gyöngyi Bárdos, Anke Claus, Veronika Ehrmann, Ina Bergheim, Andreas Schwiertz, Stephan C Bischoff
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Publicado: Public Library of Science (PLoS) 2014
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spelling oai:doaj.org-article:9518604500144c5bacb8c04c3a8bfa082021-11-18T08:35:48ZLactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.1932-620310.1371/journal.pone.0080169https://doaj.org/article/9518604500144c5bacb8c04c3a8bfa082014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24475018/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Objective</h4>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.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusions</h4>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.Yvonne RitzeGyöngyi BárdosAnke ClausVeronika EhrmannIna BergheimAndreas SchwiertzStephan C BischoffPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 1, p e80169 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Yvonne Ritze
Gyöngyi Bárdos
Anke Claus
Veronika Ehrmann
Ina Bergheim
Andreas Schwiertz
Stephan C Bischoff
Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.
description <h4>Objective</h4>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.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusions</h4>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.
format article
author Yvonne Ritze
Gyöngyi Bárdos
Anke Claus
Veronika Ehrmann
Ina Bergheim
Andreas Schwiertz
Stephan C Bischoff
author_facet Yvonne Ritze
Gyöngyi Bárdos
Anke Claus
Veronika Ehrmann
Ina Bergheim
Andreas Schwiertz
Stephan C Bischoff
author_sort Yvonne Ritze
title Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.
title_short Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.
title_full Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.
title_fullStr Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.
title_full_unstemmed Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice.
title_sort lactobacillus rhamnosus gg protects against non-alcoholic fatty liver disease in mice.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/9518604500144c5bacb8c04c3a8bfa08
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