Collaborative Metabolism: Gut Microbes Play a Key Role in Canine and Feline Bile Acid Metabolism

Rowe, John C.; Winston, Jenessa A.

doi:10.3390/vetsci11020094

Veterinary Sciences

2024

DOI: 10.3390/vetsci11020094

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Collaborative Metabolism: Gut Microbes Play a Key Role in Canine and Feline Bile Acid Metabolism

John C. Rowe,

Jenessa A. Winston

Abstract: Bile acids, produced by the liver and secreted into the gastrointestinal tract, are dynamic molecules capable of impacting the overall health of dogs and cats in many contexts. Importantly, the gut microbiota metabolizes host primary bile acids into chemically distinct secondary bile acids. This review explores the emergence of new literature connecting microbial-derived bile acid metabolism to canine and feline health and disease. Moreover, this review highlights multi-omic methodologies for translational res… Show more

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Cited by 3 publications

References 169 publications

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Bile acids impact the microbiota, host, and C. difficile dynamics providing insight into mechanisms of efficacy of FMTs and microbiota-focused therapeutics

McMillan,

Theriot

2024

Gut Microbes

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Bile acids impact the microbiota, host, and C. difficile dynamics providing insight into mechanisms of efficacy of FMTs and microbiota-focused therapeutics

McMillan,

Theriot

2024

Gut Microbes

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Fecal bile acid dysmetabolism and reduced ursodeoxycholic acid correlate with novel microbial signatures in feline chronic kidney disease

Rowe,

Summers,

Quimby

et al. 2024

Front. Microbiol.

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BackgroundMicrobial-derived secondary bile acids (SBAs) are reabsorbed and sensed via host receptors modulating cellular inflammation and fibrosis. Feline chronic kidney disease (CKD) occurs with progressive renal inflammation and fibrosis, mirroring the disease pathophysiology of human CKD patients.MethodsProspective cross-sectional study compared healthy cats (n = 6) with CKD (IRIS Stage 2 n = 17, Stage 3 or 4 n = 11). Single timepoint fecal samples from all cats underwent targeted bile acid metabolomics. 16S rRNA gene amplicon sequencing using DADA2 with SILVA taxonomy characterized the fecal microbiota.ResultsCKD cats had significantly reduced fecal concentrations (median 12.8 ng/mg, Mann–Whitney p = 0.0127) of the SBA ursodeoxycholic acid (UDCA) compared to healthy cats (median 39.4 ng/mg). Bile acid dysmetabolism characterized by <50% SBAs was present in 8/28 CKD and 0/6 healthy cats. Beta diversity significantly differed between cats with <50% SBAs and > 50% SBAs (PERMANOVA p < 0.0001). Twenty-six amplicon sequence variants (ASVs) with >97% nucleotide identity to Peptacetobacter hiranonis were identified. P. hiranonis combined relative abundance was significantly reduced (median 2.1%) in CKD cats with <50% SBAs compared to CKD cats with >50% SBAs (median 13.9%, adjusted p = 0.0002) and healthy cats with >50% SBAs (median 15.5%, adjusted p = 0.0112). P. hiranonis combined relative abundance was significantly positively correlated with the SBAs deoxycholic acid (Spearman r = 0.5218, adjusted p = 0.0407) and lithocholic acid (Spearman r = 0.5615, adjusted p = 0.0156). Three Oscillospirales ASVs and a Roseburia ASV were also identified as significantly correlated with fecal SBAs.Clinical and translational importanceThe gut-kidney axis mediated through microbial-derived SBAs appears relevant to the spontaneous animal CKD model of domestic cats. This includes reduced fecal concentrations of the microbial-derived SBA UDCA, known to regulate inflammation and fibrosis and be reno-protective. Microbes correlated with fecal SBAs include bai operon containing P. hiranonis, as well as members of Oscillospirales, which also harbor a functional bai operon. Ultimately, CKD cats represent a translational opportunity to study the role of SBAs in the gut-kidney axis, including the potential to identify novel microbial-directed therapeutics to mitigate CKD pathogenesis in veterinary patients and humans alike.

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Multi-omics reveals the alleviating effect of berberine on ulcerative colitis through modulating the gut microbiome and bile acid metabolism in the gut-liver axis

Yu,

Zheng,

Liu

et al. 2024

Front. Pharmacol.

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The dysfunction of gut microbiome and bile acid metabolism might cause the incidence and relapse of ulcerative colitis (UC). Thus, natural products have been considered effective for UC through the regulation of gut microbiome and bile acid. In this study, we evaluated the regulatory effect of berberine on gut microbiome and bile acid metabolism in UC. Results showed that the relative abundances of beneficial bacteria showed a decreasing trend in the UC model, and the taurine conjugated bile acids increased from the liver tissue to the colon tissue. Berberine inhibited the colonization of harmful bacteria and promoted the primary bile acid metabolism. Moreover, we used multi-omics technology (metagenomics, metabolomics, and transcriptomics technology) to reveal that berberine restored the intestinal barrier function through bile acid/S1PR2/RhoA/ROCK pathway. The result of transmission electron microscopy directly showed that the damaged intestinal mucosal barrier was repaired through the berberine treatment. This study revealed the treatment influence on UC through multi-omics technology in vitro and in vivo models, which provides references for explaining the mechanism of berberine on UC.

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Collaborative Metabolism: Gut Microbes Play a Key Role in Canine and Feline Bile Acid Metabolism

Cited by 3 publications

References 169 publications

Bile acids impact the microbiota, host, and C. difficile dynamics providing insight into mechanisms of efficacy of FMTs and microbiota-focused therapeutics

Bile acids impact the microbiota, host, and C. difficile dynamics providing insight into mechanisms of efficacy of FMTs and microbiota-focused therapeutics

Fecal bile acid dysmetabolism and reduced ursodeoxycholic acid correlate with novel microbial signatures in feline chronic kidney disease

Multi-omics reveals the alleviating effect of berberine on ulcerative colitis through modulating the gut microbiome and bile acid metabolism in the gut-liver axis

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