Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease

Wilson, Aze; Teft, Wendy A.; Morse, Bridget L.; Choi, Yunhee; Woolsey, Sarah; DeGorter, Marianne K.; Hegele, Robert A.; Tirona, Rommel G.; Kim, Richard B.

doi:10.1007/s10620-015-3797-3

Cited by 76 publications

(55 citation statements)

References 66 publications

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“…Wilson and colleagues studied the plasma TMAO levels in patients with IBD and ulcerative colitis (UC) and found them to be lower in the IBD patients (2.27 μM) compared with the healthy individuals. Similarly, lower TMAO levels were observed in patients with active UC (1.56 μM) versus inactive disease (3.40 μM) (Wilson et al, ; Wilson et al, ). In an experimental study, Van Hecke and colleagues studied the effect of white versus red meat consumption on oxidative stress, TMAO and inflammation in Sprague–Dawley rats.…”

Section: Tmao Enhances the Risk Of Inflammation Obesity And Atherosmentioning

confidence: 90%

“…Although gut microbiota appears to have both positive and negative effects on our health, most of those which exist in the large intestine, process many indigestible components of foods and convert them into 10% of our daily energy supply. ‘New Age’ foods rich in calories with reduced fibre, facilitate the aberrant expansion of Proteobacteria, as observed in both inflammatory bowel disease (IBD) and metabolic disorders (Wilson et al, ; Wilson et al, ). Particularly, an increased ratio of Firmicutes / Bacteroidetes has been associated with a high risk of cardiovascular disease (CVD; Abdallah Ismail et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Trimethylamine N‐oxide: breathe new life

Subramaniam

Fletcher

2017

British J Pharmacology

143

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Section: Tmao Enhances the Risk Of Inflammation Obesity And Atherosmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Trimethylamine N‐oxide: breathe new life

Subramaniam

Fletcher

2017

British J Pharmacology

143

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“…TMAO is produced by gastrointestinal anaerobes through the digestion of dietary phosphatidylcholine and carnitine in a microbial–mammalian co-metabolic pathway and might serve as a biomarker for IBD (Wilson et al 2015). In this study, the increased urinary concentration of TMAO might be due to the successful colonization of anaerobic bacteria in the gut after FMT.…”

Section: Discussionmentioning

confidence: 99%

Timing for the second fecal microbiota transplantation to maintain the long-term benefit from the first treatment for Crohn’s disease

Zhang

Xiao

et al. 2018

Appl Microbiol Biotechnol

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Increasing evidence has shown that fecal microbiota transplantation (FMT) could be a promising treatment option for Crohn’s disease (CD). However, the frequency of FMT for CD treatment remains unclear. This study aimed to evaluate the optimal timing for administering the second course of FMT to maintain the long-term clinical effects from the first FMT for patients with CD. Sixty-nine patients with active CD who underwent FMT twice and benefited from the first FMT were enrolled in this study. Clinical response, stool microbiota, and urine metabolome of patients were assessed during the follow-up. The median time of maintaining clinical response to the first FMT in total 69 patients was 125 days (IQR, 82.5–225.5). The time of maintaining clinical response to the second FMT in 56 of 69 patients was 176.5 days (IQR, 98.5–280). The fecal microbiota composition of each patient post the first FMT was closer to that of his/her donor. Compared to that of the baseline, patients prior to the second course of FMT showed significant differences in urinary metabolic profiles characterized by increased indoxyl sulfate, 4-hydroxyphenylacetate, creatinine, dimethylamine, glycylproline, hippurate, and trimethylamine oxide (TMAO). This study demonstrated that patients with CD could be administered the second course of FMT less than 4 months after the first FMT for maintaining the clinical benefits from the first FMT. This was supported by the host–microbial metabolism changes in patients with active CD. Trial registration: ClinicalTrials.gov, NCT01793831. Registered 18 February 2013. https://clinicaltrials.gov/ct2/show/NCT01793831?term=NCT01793831&rank=1Electronic supplementary materialThe online version of this article (10.1007/s00253-018-9447-x) contains supplementary material, which is available to authorized users.

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“…Likewise, fecal levels of medium-chain fatty acids were reported to be decreased in patients with UC, Crohn’s disease, or pouchitis; fecal concentrations of hexanoate correlated inversely with disease activity 123 . Levels of trimethylamine-N-oxide, produced by bacterial metabolism of dietary carnitine and phosphatidylcholine followed by hepatic metabolism, are decreased in plasma samples from patients with IBD vs controls and correlate with activity of UC but not Crohn’s disease 132 .…”

Section: Microbiota In Development and Progression Of Ibdmentioning

confidence: 98%

Roles for Intestinal Bacteria, Viruses, and Fungi in Pathogenesis of Inflammatory Bowel Diseases and Therapeutic Approaches

2017

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Intestinal microbiota are involved in the pathogenesis of Crohn’s disease, ulcerative colitis, and pouchitis. We review the mechanisms by which these gut bacteria, fungi, and viruses mediate mucosal homeostasis, via their composite genes (metagenome) and metabolic products (metabolome). We explain how alterations to their profiles and functions under conditions of dysbiosis contribute to inflammation and effector immune responses that mediate inflammatory bowel diseases (IBD) in humans and enterocolitis in mice. It could be possible to engineer the intestinal environment by modifying the microbiota community structure or function to treat patients with IBD— either with individual agents, via dietary management, or as adjuncts to immunosuppressive drugs. We summarize the latest information on therapeutic use of fecal microbial transplantation and propose improved strategies to selectively normalize the dysbiotic microbiome in personalized approaches to treatment.

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Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease

Abstract: Decreased TMAO levels are seen in IBD compared to a non-IBD population. These data suggest that TMAO may have potential as a biomarker to support IBD diagnosis as well as to assess disease activity in UC.

Cited by 76 publications

References 66 publications

Trimethylamine N‐oxide: breathe new life

Trimethylamine N‐oxide: breathe new life

Timing for the second fecal microbiota transplantation to maintain the long-term benefit from the first treatment for Crohn’s disease

Roles for Intestinal Bacteria, Viruses, and Fungi in Pathogenesis of Inflammatory Bowel Diseases and Therapeutic Approaches

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