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Auteur D. S. HITTEL |
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Ketogenic diet modifies the gut microbiota in a murine model of autism spectrum disorder / C. NEWELL in Molecular Autism, 7 (2016)
[article]
Titre : Ketogenic diet modifies the gut microbiota in a murine model of autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : C. NEWELL, Auteur ; M. R. BOMHOF, Auteur ; R. A. REIMER, Auteur ; D. S. HITTEL, Auteur ; J. M. RHO, Auteur ; J. SHEARER, Auteur Article en page(s) : 37p. Langues : Anglais (eng) Mots-clés : Animals Autism Spectrum Disorder/microbiology Bacteria/isolation & purification Behavior, Animal Cecum/microbiology Diet, Ketogenic Disease Models, Animal Feces/microbiology Gastrointestinal Microbiome Male Mice Mice, Inbred C57BL Social Behavior Autism spectrum disorder BTBR mouse Gut microbiome Ketogenic diet Index. décimale : PER Périodiques Résumé : BACKGROUND: Gastrointestinal dysfunction and gut microbial composition disturbances have been widely reported in autism spectrum disorder (ASD). This study examines whether gut microbiome disturbances are present in the BTBR(T + tf/j) (BTBR) mouse model of ASD and if the ketogenic diet, a diet previously shown to elicit therapeutic benefit in this mouse model, is capable of altering the profile. FINDINGS: Juvenile male C57BL/6 (B6) and BTBR mice were fed a standard chow (CH, 13 % kcal fat) or ketogenic diet (KD, 75 % kcal fat) for 10-14 days. Following diets, fecal and cecal samples were collected for analysis. Main findings are as follows: (1) gut microbiota compositions of cecal and fecal samples were altered in BTBR compared to control mice, indicating that this model may be of utility in understanding gut-brain interactions in ASD; (2) KD consumption caused an anti-microbial-like effect by significantly decreasing total host bacterial abundance in cecal and fecal matter; (3) specific to BTBR animals, the KD counteracted the common ASD phenotype of a low Firmicutes to Bacteroidetes ratio in both sample types; and (4) the KD reversed elevated Akkermansia muciniphila content in the cecal and fecal matter of BTBR animals. CONCLUSIONS: Results indicate that consumption of a KD likely triggers reductions in total gut microbial counts and compositional remodeling in the BTBR mouse. These findings may explain, in part, the ability of a KD to mitigate some of the neurological symptoms associated with ASD in an animal model. En ligne : http://dx.doi.org/10.1186/s13229-016-0099-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328
in Molecular Autism > 7 (2016) . - 37p.[article] Ketogenic diet modifies the gut microbiota in a murine model of autism spectrum disorder [Texte imprimé et/ou numérique] / C. NEWELL, Auteur ; M. R. BOMHOF, Auteur ; R. A. REIMER, Auteur ; D. S. HITTEL, Auteur ; J. M. RHO, Auteur ; J. SHEARER, Auteur . - 37p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 37p.
Mots-clés : Animals Autism Spectrum Disorder/microbiology Bacteria/isolation & purification Behavior, Animal Cecum/microbiology Diet, Ketogenic Disease Models, Animal Feces/microbiology Gastrointestinal Microbiome Male Mice Mice, Inbred C57BL Social Behavior Autism spectrum disorder BTBR mouse Gut microbiome Ketogenic diet Index. décimale : PER Périodiques Résumé : BACKGROUND: Gastrointestinal dysfunction and gut microbial composition disturbances have been widely reported in autism spectrum disorder (ASD). This study examines whether gut microbiome disturbances are present in the BTBR(T + tf/j) (BTBR) mouse model of ASD and if the ketogenic diet, a diet previously shown to elicit therapeutic benefit in this mouse model, is capable of altering the profile. FINDINGS: Juvenile male C57BL/6 (B6) and BTBR mice were fed a standard chow (CH, 13 % kcal fat) or ketogenic diet (KD, 75 % kcal fat) for 10-14 days. Following diets, fecal and cecal samples were collected for analysis. Main findings are as follows: (1) gut microbiota compositions of cecal and fecal samples were altered in BTBR compared to control mice, indicating that this model may be of utility in understanding gut-brain interactions in ASD; (2) KD consumption caused an anti-microbial-like effect by significantly decreasing total host bacterial abundance in cecal and fecal matter; (3) specific to BTBR animals, the KD counteracted the common ASD phenotype of a low Firmicutes to Bacteroidetes ratio in both sample types; and (4) the KD reversed elevated Akkermansia muciniphila content in the cecal and fecal matter of BTBR animals. CONCLUSIONS: Results indicate that consumption of a KD likely triggers reductions in total gut microbial counts and compositional remodeling in the BTBR mouse. These findings may explain, in part, the ability of a KD to mitigate some of the neurological symptoms associated with ASD in an animal model. En ligne : http://dx.doi.org/10.1186/s13229-016-0099-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328