Intestinal flora and bilirubin

Tiribelli, Claudio; Ostrow, J. Donald

doi:10.1016/j.jhep.2004.12.002

Cited by 28 publications

(23 citation statements)

References 31 publications

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“…The degradation of bilirubin occurs through intestinal bacteria such as Clostridium spp. (Tiribelli and Ostrow, 2005). However, also one further phenolic compound seems to have an important role in discriminating C57J and C57N mice.…”

Section: Discussionmentioning

confidence: 97%

Distinct signatures of host–microbial meta-metabolome and gut microbiome in two C57BL/6 strains under high-fat diet

et al. 2014

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A combinatory approach using metabolomics and gut microbiome analysis techniques was performed to unravel the nature and specificity of metabolic profiles related to gut ecology in obesity. This study focused on gut and liver metabolomics of two different mouse strains, the C57BL/6J (C57J) and the C57BL/6N (C57N) fed with high-fat diet (HFD) for 3 weeks, causing dietinduced obesity in C57N, but not in C57J mice. Furthermore, a 16S-ribosomal RNA comparative sequence analysis using 454 pyrosequencing detected significant differences between the microbiome of the two strains on phylum level for Firmicutes, Deferribacteres and Proteobacteria that propose an essential role of the microbiome in obesity susceptibility. Gut microbial and liver metabolomics were followed by a combinatory approach using Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS) and ultra performance liquid chromatography time of tlight MS/MS with subsequent multivariate statistical analysis, revealing distinctive host and microbial metabolome patterns between the C57J and the C57N strain. Many taurine-conjugated bile acids (TBAs) were significantly elevated in the cecum and decreased in liver samples from the C57J phenotype likely displaying different energy utilization behavior by the bacterial community and the host. Furthermore, several metabolite groups could specifically be associated with the C57N phenotype involving fatty acids, eicosanoids and urobilinoids. The mass differences based metabolite network approach enabled to extend the range of known metabolites to important bile acids (BAs) and novel taurine conjugates specific for both strains. In summary, our study showed clear alterations of the metabolome in the gastrointestinal tract and liver within a HFD-induced obesity mouse model in relation to the host-microbial nutritional adaptation.

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Section: Discussionmentioning

confidence: 97%

Distinct signatures of host–microbial meta-metabolome and gut microbiome in two C57BL/6 strains under high-fat diet

et al. 2014

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“…Calculations are based on the assumption that quantitative disposal of bilirubin and its derivatives from the body occurs exclusively via the feces; i.e., fecal excretion of UCB plus derivatives equals fractional bilirubin turnover from the UCB pool. This assumption seems reasonable, since, in Gunn rats, urinary secretion of labeled UCB and its derivatives (consisting of polar photoderivatives, urobilinoids and other bacterial metabolites) is limited (5%) (10,22). Our calculations are also based on the assumption that metabolism of UCB to UCBderivatives quantitatively occurs only in the intestinal lumen.…”

Section: Discussionmentioning

confidence: 99%

Novel Kinetic Insights into Treatment of Unconjugated Hyperbilirubinemia: Phototherapy and Orlistat Treatment in Gunn Rats

et al. 2006

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ABSTRACT:Treatment with phototherapy or with the lipase inhibitor orlistat decreases plasma unconjugated bilirubin (UCB) concentrations in hyperbilirubinemic Gunn rats. We investigated the mechanism(s) underlying the effects of orlistat, phototherapy, and combined treatment, using steady-state 3 H-UCB kinetics. After three weeks of treatment with orlistat (200 mg/kg chow), phototherapy (19 W/cm 2 /nm) or combined treatment, tracer 3 H-UCB was administered IV to treated and untreated (control) Gunn rats. Plasma samples and feces were collected every 12h for 60h, and bile for 30 min at 60h. The following results were obtained: 1) each treatment decreased plasma bilirubin levels compared with controls: orlistat-19%, phototherapy-32%, combined treatment-53%; 2) plasma bilirubin concentrations were strongly, negatively correlated with fractional bilirubin turnover; 3) orlistat treatment induced net transmucosal excretion of UCB into the intestinal lumen, whereas phototherapy increased biliary UCB excretion rate; 4) all treatments profoundly increased the enterohepatic circulation of UCB derivatives, indicating enhanced metabolism by intestinal bacteria. In conclusion, orlistat and phototherapy lower plasma bilirubin concentrations in Gunn rats by increasing (net) intestinal influx of UCB, either by transmucosal excretion (orlistat), or increased biliary secretion (phototherapy). The mechanism of phototherapy and orlistat treatment involves increasing the availability of UCB in the intestinal lumen for fecal excretion and for metabolism by intestinal bacteria.

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“…The same process is also true for UCB, which can be, under certain conditions, also reabsorbed. A small portion of UCB is reabsorbed in the colon and delivered back to liver by portal circulation …”

Section: A Review Of Bilirubin Metabolismmentioning

confidence: 99%

“…11 Within the intestinal lumen (Fig 1), almost all bilirubin is deconjugated; part is excreted as UCB, but the majority is excreted as urobilinoids. 12 Beta-glucuronidase first deconjugates CB to UCB, which is then reduced to urobilinogen and stercobilinogen by the microbiota, being almost absent at birth and needing 6-12 month to stably populate the intestine. [13][14][15] After oxidation, stercobilin and urobilin are excreted via faeces.…”

Section: The Sinusoidal Liver-to-blood Loop (Figure 2)mentioning

confidence: 99%

See 1 more Smart Citation

The molecular basis of jaundice: An old symptom revisited

Gazzin

Masutti

Vı́tek

et al. 2017

Liver International

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Increased serum bilirubin level is a widely used diagnostic marker for hepatic illnesses. Nevertheless, mild elevation of unconjugated serum bilirubin (such as in Gilbert syndrome) has been recently demonstrated to correlate with low risk of chronic inflammatory and/or oxidative stress-mediated diseases. In accord, a low serum bilirubin level has emerged as an important predisposing factor or a biomarker of these pathologic conditions including cardiovascular, tumour, and possibly neurodegenerative diseases. Bilirubin possesses multiple biological actions with interaction in a complex network of enzymatic and signalling pathways. The fact that the liver is the main organ controlling the bioavailability of bilirubin emphasizes the central role of this organ in human health.

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Intestinal flora and bilirubin

Cited by 28 publications

References 31 publications

Distinct signatures of host–microbial meta-metabolome and gut microbiome in two C57BL/6 strains under high-fat diet

Distinct signatures of host–microbial meta-metabolome and gut microbiome in two C57BL/6 strains under high-fat diet

Novel Kinetic Insights into Treatment of Unconjugated Hyperbilirubinemia: Phototherapy and Orlistat Treatment in Gunn Rats

The molecular basis of jaundice: An old symptom revisited

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