Chronic diarrhea, bile acids, and Clostridia
Julian R.F. Walters1,2 and Julian R. Marchesi1,3
1Division of Digestive Diseases, Department of Metabolism, Digestion, and Reproduction, Faculty of Medicine, Imperial College London, London, United Kingdom.
2Gastroenterology, Division of Medicine and Integrated Care, Imperial College Healthcare NHS Trust, London, United Kingdom.
3School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Address correspondence to: Julian Walters, Division of Digestive Diseases, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0HS, United Kingdom. Phone: 44.203.313.2361; Email: julian.walters@imperial.ac.uk.
Find articles by Walters, J. in: JCI | PubMed | Google Scholar
1Division of Digestive Diseases, Department of Metabolism, Digestion, and Reproduction, Faculty of Medicine, Imperial College London, London, United Kingdom.
2Gastroenterology, Division of Medicine and Integrated Care, Imperial College Healthcare NHS Trust, London, United Kingdom.
3School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Address correspondence to: Julian Walters, Division of Digestive Diseases, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0HS, United Kingdom. Phone: 44.203.313.2361; Email: julian.walters@imperial.ac.uk.
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Published December 9, 2019 - More info
J Clin Invest. 2020;130(1):77–79. https://doi.org/10.1172/JCI133117.
© 2020 American Society for Clinical Investigation
Excessive fecal bile acid (BA) loss causes symptoms in a large proportion of people diagnosed with irritable bowel syndrome with diarrhea, a common functional bowel disorder. This BA diarrhea (BAD) results from increased hepatic synthesis of BAs, with impaired negative feedback regulation by the ileal hormone fibroblast growth factor 19 (FGF19). In this issue of the JCI, Zhao et al. investigated BA metabolism, including fecal BAs, serum BAs, and FGF19, in patients and controls. They identified associations between fecal bacterial BA metabolism and specific microbiota, especially Clostridium scindens. These findings have been tested in a mouse model using microbiota transplants and antibiotic treatment. This group of organisms has potential as a biomarker for BAD and to be a target for therapy.
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