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Review
. 2017 Jan;101(1):47-64.
doi: 10.1007/s00253-016-8006-6. Epub 2016 Nov 25.

Interaction of gut microbiota with bile acid metabolism and its influence on disease states

Affiliations
Review

Interaction of gut microbiota with bile acid metabolism and its influence on disease states

VSports注册入口 - Christopher Staley et al. Appl Microbiol Biotechnol. 2017 Jan.

Abstract (V体育官网入口)

Primary bile acids serve important roles in cholesterol metabolism, lipid digestion, host-microbe interactions, and regulatory pathways in the human host. While most bile acids are reabsorbed and recycled via enterohepatic cycling, ∼5% serve as substrates for bacterial biotransformation in the colon. Enzymes involved in various transformations have been characterized from cultured gut bacteria and reveal taxa-specific distribution. More recently, bioinformatic approaches have revealed greater diversity in isoforms of these enzymes, and the microbial species in which they are found. Thus, the functional roles played by the bile acid-transforming gut microbiota and the distribution of resulting secondary bile acids, in the bile acid pool, may be profoundly affected by microbial community structure and function. Bile acids and the composition of the bile acid pool have historically been hypothesized to be associated with several disease states, including recurrent Clostridium difficile infection, inflammatory bowel diseases, metabolic syndrome, and several cancers VSports手机版. Recently, however, emphasis has been placed on how microbial communities in the dysbiotic gut may alter the bile acid pool to potentially cause or mitigate disease onset. This review highlights the current understanding of the interactions between the gut microbial community, bile acid biotransformation, and disease states, and addresses future directions to better understand these complex associations. .

Keywords: Bile acids; C V体育安卓版. difficile; Dysbiosis; Host-interactions; Microbial metabolism. .

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Figures

Figure 1
Figure 1
Bile acid synthesis pathway in humans. Green arrows reflect the primary process of bile acid synthesis while blue arrows show an alternative pathway.
Figure 2
Figure 2
Overview of enterohepatic circulation and microbial processing of bile acids. Gray arrows indicate host processes, and thick black arrows reflect processes performed by the microbiome. Thin, solid arrows reflect the direction of primary acid flow while dashed arrows reflect secondary bile acids. Open symbols reflect passive transport. BA: bile acid, G: glycine, T: taurine.
Figure 3
Figure 3
Chemical structures of secondary bile acids derived from (A) cholic acid and (B) chenodeoxycholic acid.
Figure 4
Figure 4
Bile acid composition in the colon and Cl. difficile infection. Right panel: Following antibiotic treatment, the proportion of primary bile acids, including CA, TCA, and CDCA, increases in the colon and feces, along with susceptibility to CDI, possibly by allowing Cl. difficile spores to germinate into vegetative cells (dark blue). (Left panel: An FMT can reverse these effects, increasing the proportion of secondary bile acids, such as DCA and LCA, in the feces, and prevent recurrence of CDI, possibly by inhibiting germination of Cl. difficile spores (light blue). CA: cholic acid; TCA: taurocholic acid; CDCA: chenodeoxycholic acid; DCA: deoxycholic acid; LCA: lithocholic acid; FMT: fecal microbiota transplantation. Modified from93.
Figure 5
Figure 5
Effects of diet, bile acids, host genetics, and intestinal bacteria on colitis. In genetically susceptible mice (IL-10-/-), a diet rich in milk fat increases taurocholic acid production, which in turn increases the abundance of sulfite-producing bacteria in the colon. Together these factors increase intestinal inflammation.
Figure 6
Figure 6
Bacterial bile acid metabolism can influence metabolic syndrome. Expression of bile salt hydrolase (BSH) by E. coli increases deconjugation of taurocholic acid (TCA) to cholic acid (CA), which increases FXR activation to alter gene expression associated with lipid digestion, adiposignaling, immune-homeostasis, and circadian rhythms, ultimately leading to decreased liver triglycerides and decreased weight gain in the host.

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