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We read with interest the informative and required investigation of bile-acid dysmetabolism, dysbiosis and inflammation in inflammatory bowel diseases (IBD) by Duboc et al.1 The paper suggests that a characteristic finding of IBD is reduced faecal secondary bile acids (BA), increased conjugated BA and increased sulphated BA.1 The authors link the luminal dysmetabolism of BA to dysbiosis, and the loss of microbiota deconjugation, transformation and desulphation enzymatic functions.1 The authors report convincing evidence demonstrating that a decrease in bacteria-bearing bile salt hydrolase (BSH) activities may be involved in the increase in conjugated BA remaining in the faeces, and show that germ-free mice have a similar loss of microbiota enzymatic function and display similar faecal BA irregularities.1 In addition to their role in dietary lipid absorption, BA are signalling modules activating nuclear receptors, including the farnesoid-X-receptor, the constitutive androstane receptor, the pregnane-X-receptor and the vitamin D receptor (VDR), as well as the …
Contributors MLJ, SP and CJM designed the study and prepared the letter. All authors have read and approved the final manuscript.
Funding This work was supported by Micropharma Limited.
Competing interests MLJ and SP acknowledge a conflict of interest as they are cofounders and shareholders of Micropharma. CJM is employed by, and is a shareholder of, Micropharma.
Patient consent Obtained.
Ethics approval The study was conducted according to the principles of the Declaration of Helsinki. Otherwise healthy hypercholesterolemic adults were recruited from six centres in Prague, Czech Republic. The protocol was approved by the Ethics Committee for multicentric clinical trials of the University Hospital Motol, Czech Republic (FDA/OHRP IORG registration no. IORG0000612). The trial was registered on www.clinicaltrials.gov under study number NCT01341613.
Provenance and peer review Not commissioned; internally peer reviewed.
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