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Secreted factors of Lactobacillus rhamnosus GG culture prevents chronic alcohol‐induced liver injury
Author(s) -
Wang Yuhua,
Wang Cuiling,
Wang Chunhong,
Zhang Min,
Liu Yanlong,
McClain Craig,
Feng Wenke
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1106.1
Subject(s) - ampk , medicine , liquid diet , steatosis , endocrinology , liver injury , lactobacillus rhamnosus , amp activated protein kinase , apoptosis , triglyceride , alcohol , intestinal permeability , biology , chemistry , phosphorylation , biochemistry , protein kinase a , lactobacillus , cholesterol , fermentation
Lactobacillus rhamnosus GG (LGG) culture supernatant (LGGs) ameliorated acute alcohol‐induced intestinal permeability and liver injury. We examined whether LGGs provides a protective effect. Mice were fed diet containing 5% alcohol for 4 weeks, and LGGs was administered at a dose of equivalent to 10 9 CFU/mouse with alcohol. LGGs decreased chronic alcohol‐induced plasma LPS concentration, increased expression of mucus factors and tight junctions, and decreased intestinal permeability. LGGs decreased chronic alcohol‐induced liver injury evaluated by ALT in plasma. Alcohol‐induced hepatic steatosis was prevented by LGGs evaluated by triglyceride contents and Oil Red O staining. Alcohol decreased AMPK and ACC phosphorylation and CPT‐1 expression, and these effects were prevented by LGGs administration in vivo and in cell culture. Inhibition of AMPK phosphorylation by Compound C abolished LGGs‐induced ACC inactivation and CPT‐1 up‐regulation, suggesting that the protective effect of LGGs on lipid metabolism in response to alcohol exposure is mediated via AMPK pathway. LGGs prevented alcohol‐induced hepatic apoptosis evaluated by TUNEL assay. These results suggest that LGGs is effective in preventing chronic alcohol‐induced liver injury by promoting intestinal integrity and attenuating hepatic apoptosis, and increasing lipid β‐oxidation through AMPK phosphorylation.