Lactulose drives a reversible reduction and qualitative modulation of the faecal microbiota diversity in healthy dogs

Marisa da Fonseca Ferreira*, Silke Salavati Schmitz, Jeffrey Joseph Schoenebeck, Dylan Neil Clements, Susan Mary Campbell, Donna Elaine Gaylor, Richard J. Mellanby, Adam George Gow, Mazdak Salavati

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)


Hepatic encephalopathy is a frequent and debilitating complication of liver disorders. Lactulose is an established and reasonably effective treatment, yet with incompletely understood mechanisms of action. The aims of this study were to examine how the faecal microbiota composition changed before, during and after lactulose treatment in a large animal model. Healthy, privately owned dogs (n = 18) completed a prospective cohort study. Faecal samples were collected weekly, while the subjects were either on their usual diet (week 1), or a standardised diet (weeks 2–9), with added oral lactulose in weeks 6–7. DNA extraction and 16S rRNA gene sequencing were undertaken. Faecal samples from week 7 had a significantly lower microbiota richness/diversity, based on observed operational taxonomic units, Shannon/Chao1 indexes and Pielou’s Evenness. Beta diversity based on UniFrac distances was significantly different in week 7 compared to weeks 1, 5 and 9. At the phylum level, week 7 was associated with a significant increase of Firmicutes and Actinobacteria, and a decrease of Bacteroidetes and Fusobacteria, when compared to weeks 5 and 9. In summary, we have shown that lactulose induces a reversible qualitative and quantitative change of the faecal microbiota, which may explain its clinical efficacy in the management of hepatic encephalopathy.

Original languageEnglish
Article number13350
JournalScientific Reports
Issue number1
Publication statusPrint publication - 16 Sept 2019
Externally publishedYes

Bibliographical note

Funding Information:
The authors would like to thank Edinburgh Genomics, The University of Edinburgh, for performing the DNA sequencing and generating the raw data. Edinburgh Genomics is partly supported through core grants from NERC (R8/H10/56), MRC (MR/K001744/1) and BBSRC (BB/J004243/1). The authors would also like to thank the owners who consented their dogs to participate in this study. This study was supported by a Royal (Dick) School of Veterinary Studies Clinical Research Grant. The funding source had no involvement in: the study design; the collection, analysis and interpretation of data; the writing of the manuscript; or the decision to submit the manuscript for publication. J.J.S. is a University of Edinburgh Chancellor’s Fellow based at the Roslin Institute. He is supported by strategic funding from the Biotechnology and Biosciences Research Council (BB/P013759/1 and BB/P013732/1). R.J.M. and M.S. were supported by BBSRC through the Institute Strategic Programme funding (BB/J004235/1 and BB/P013740/1).

Publisher Copyright:
© 2019, The Author(s).


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