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Lactobacillus acidophilus DDS-1 modulates the gut microbiota and improves metabolic profiles in aging mice

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Vemuri, RC ORCID: 0000-0002-3238-426X, Shinde, TS ORCID: 0000-0002-8551-5841, Gundamaraju, R, Gondalia, SV, Karpe, AV, Beale, DJ, Martoni, CJ and Eri, R ORCID: 0000-0003-1688-8043 2018 , 'Lactobacillus acidophilus DDS-1 modulates the gut microbiota and improves metabolic profiles in aging mice' , Nutrients, vol. 10, no. 9 , pp. 1-19 , doi: 10.3390/nu10091255.

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Abstract

Recent evidence suggests that gut microbiota shifts can alter host metabolism even during healthy aging. Lactobacillus acidophilus DDS-1, a probiotic strain, has shown promising probiotic character in vitro, as well as in clinical studies. The present study was carried out to investigate whether DDS-1 can modulate the host metabolic phenotype under the condition of age-affected gut microbial shifts in young and aging C57BL/6J mice. Collected fecal samples were analyzed using 16S rRNA gene sequencing for identifying gut microbiota and untargeted gas chromatography-mass spectrometry (GC-MS) metabolomics analysis. Gut microbial shifts were observed in the control groups (young and aging), leading to an alteration in metabolism. Principal coordinate analysis (PCoA) of microbiota indicated distinct separation in both the DDS-1-treated groups. L. acidophilus DDS-1 increased the relative abundances of beneficial bacteria, such as Akkermansia muciniphila and Lactobacillus spp., and reduced the relative levels of opportunistic bacteria such as Proteobacteria spp. Metabolic pathway analysis identified 10 key pathways involving amino acid metabolism, protein synthesis and metabolism, carbohydrate metabolism, and butanoate metabolism. These findings suggest that modulation of gut microbiota by DDS-1 results in improvement of metabolic phenotype in the aging mice.

Item Type: Article
Authors/Creators:Vemuri, RC and Shinde, TS and Gundamaraju, R and Gondalia, SV and Karpe, AV and Beale, DJ and Martoni, CJ and Eri, R
Journal or Publication Title: Nutrients
Publisher: MDPI Publishing
ISSN: 2072-6643
DOI / ID Number: 10.3390/nu10091255
Copyright Information:

Copyright 2018 The Authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/

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