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Prebiotic approach alleviates hepatic steatosis: Implication of fatty acid oxidative and cholesterol synthesis pathways
Author(s) -
Pachikian Barbara D.,
Essaghir Ahmed,
Demoulin JeanBaptiste,
Catry Emilie,
Neyrinck Audrey M.,
Dewulf Evelyne M.,
Sohet Florence M.,
Portois Laurence,
Clerbaux LaureAlix,
Carpentier Yvon A.,
Possemiers Sam,
Bommer Guido T.,
Cani Patrice D.,
Delzenne Nathalie M.
Publication year - 2013
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201200364
Subject(s) - steatosis , fatty liver , medicine , endocrinology , beta oxidation , gut flora , biology , lipid metabolism , triglyceride , cholesterol , metabolism , biochemistry , disease
Scope Recent data suggest that gut microbiota contributes to the regulation of host lipid metabolism. We report how fermentable dietary fructo‐oligosaccharides ( FOS ) control hepatic steatosis induced by n ‐3 PUFA depletion, which leads to hepatic alterations similar to those observed in non‐alcoholic fatty liver disease patients. Methods and results C57Bl/6J mice fed an n ‐3 PUFA‐depleted diet for 3 months were supplemented with FOS during the last 10 days of treatment. FOS‐treated mice exhibited higher caecal B ifidobacterium spp. and lower R oseburia spp. content. Microarray analysis of hepatic m RNA revealed that FOS supplementation reduced hepatic triglyceride accumulation through a proliferator‐activated receptor α‐stimulation of fatty acid oxidation and lessened cholesterol accumulation by inhibiting sterol regulatory element binding protein 2‐dependent cholesterol synthesis. Cultured precision‐cut liver slices confirmed the inhibition of fatty acid oxidation. FOS effects were related to a decreased hepatic micro‐ RNA 33 expression and to an increased colonic glucagon‐like peptide 1 production. Conclusions The changes in gut microbiota composition by n ‐3 PUFA‐depletion and prebiotics modulate hepatic steatosis by changing gene expression in the liver, a phenomenon that could implicate micro‐ RNA and gut‐derived hormones. Our data underline the advantage of targeting the gut microbiota by colonic nutrients in the management of liver disease.