The gut microbiome-bile acid axis in hepatocarcinogenesis

Wu, Liwei; Jiao, Feng; Li, Jingjing; Yu, Qiang; Ji, Jie; Wu, Jianye; Dai, Weiqi; Guo, Chuanyong

doi:10.1016/j.biopha.2020.111036

Cited by 57 publications

(71 citation statements)

References 134 publications

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“…Our results showed that ALS treatment not only led to the enrichment of BAs, such as LCA, DCA, and CDCA, but also the activation of FXR signaling in the colon. Recent work described that the biotransformation of BAs due to gut microbiota can impact the metabolism of BAs in the liver [40]. Our results showed a trend toward increased Cyp7a1 but not FXR.…”

Section: Discussionsupporting

confidence: 54%

Armillaria luteo-virens Sacc Ameliorates Dextran Sulfate Sodium Induced Colitis through Modulation of Gut Microbiota and Microbiota-Related Bile Acids

et al. 2021

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Armillaria luteo-virens Sacc (ALS) is a rare wild Chinese medicinal and edible basidiomycete. However, its protective effect on intestinal functions and the underlying mechanism is still unknown. This work explored the improvement of dextran sulfate sodium (DSS)-induced colitis by ALS. ALS supplementation markedly improved colitis symptoms, gut barrier integrity, and goblet loss in DSS-treated mice. In addition, ALS inhibited colonic inflammation through the inhibition/activation of the mitogen-activated protein kinases/NF-κB signaling pathway. The 16S rRNA gene-based microbiota analysis revealed that ALS altered the gut microbiota composition, decreasing the richness of Enterobacteriaceae and increasing the abundance of Lactobacillaceae. The bile-acid-targeted metabolomic analysis showed that ALS recovered the microbial bile acid metabolism in the gut, enabling the activation of the farnesoid X receptor signaling by these acids, thus maintaining the intestinal homeostasis. Importantly, broad-spectrum antibiotic treatment reduced the efficacy of ALS-induced protection from colitis. Overall, our findings suggest that ALS may represent a novel approach in the nutritional intervention to prevent colitis.

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Section: Discussionsupporting

confidence: 54%

Armillaria luteo-virens Sacc Ameliorates Dextran Sulfate Sodium Induced Colitis through Modulation of Gut Microbiota and Microbiota-Related Bile Acids

et al. 2021

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“…But other studies suggest potentially protective roles for taurine‐conjugated BA in the presence of cardiometabolic risk factors 36 —something that deserves further investigation in relation to liver diseases. BA deconjugation and production of secondary BAs is dependent on the gut bacterial microbiome 8 . Interestingly, Petrick et al observed an inverse HCC risk association between secondary BA and HCC risk in chronic hepatitis patients, 22 also possibly implicating alterations in the bacterial microbiome composition, something that has previously been observed during hepatitis infections 37,38 .…”

Section: Discussionmentioning

confidence: 90%

“…But, they can also promote cell proliferation, inflammation and oxidative stress, potentially leading to DNA damage and tumor growth 6,7 . Primary BAs are synthesized in the liver, conjugated with taurine or glycine and stored in the gall bladder as bile which is excreted into the intestinal tract with food consumption 8 . Excreted BAs are largely deconjugated, the majority are reabsorbed via the entero‐hepatic circulation and some reach the colon where they are converted to secondary BA by gut microbial action before also being largely reabsorbed 8 …”

Section: Introductionmentioning

confidence: 99%

Prediagnostic alterations in circulating bile acid profiles in the development of hepatocellular carcinoma

Stępień

López-Nogueroles

Lahoz

et al. 2022

Intl Journal of Cancer

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Bile acids (BAs) play different roles in cancer development. Some are carcinogenic and BA signaling is also involved in various metabolic, inflammatory and immune‐related processes. The liver is the primary site of BA synthesis. Liver dysfunction and microbiome compositional changes, such as during hepatocellular carcinoma (HCC) development, may modulate BA metabolism increasing concentration of carcinogenic BAs. Observations from prospective cohorts are sparse. We conducted a study (233 HCC case‐control pairs) nested within a large observational prospective cohort with blood samples taken at recruitment when healthy with follow‐up over time for later cancer development. A targeted metabolomics method was used to quantify 17 BAs (primary/secondary/tertiary; conjugated/unconjugated) in prediagnostic plasma. Odd ratios (OR) for HCC risk associations were calculated by multivariable conditional logistic regression models. Positive HCC risk associations were observed for the molar sum of all BAs (ORdoubling = 2.30, 95% confidence intervals [CI]: 1.76‐3.00), and choline‐ and taurine‐conjugated BAs. Relative concentrations of BAs showed positive HCC risk associations for glycoholic acid and most taurine‐conjugated BAs. We observe an association between increased HCC risk and higher levels of major circulating BAs, from several years prior to tumor diagnosis and after multivariable adjustment for confounders and liver functionality. Increase in BA concentration is accompanied by a shift in BA profile toward higher proportions of taurine‐conjugated BAs, indicating early alterations of BA metabolism with HCC development. Future studies are needed to assess BA profiles for improved stratification of patients at high HCC risk and to determine whether supplementation with certain BAs may ameliorate liver dysfunction.

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“…As pointed out already, dysbiosis influences the gut barrier and bile acid composition and leads to fibrosis and cirrhosis [91,121]. Furthermore, dysbiosis also takes part in the promotion of carcinogenesis of hepatocellular cancer [177]. Alterations of the microbiome have been shown for cholestatic liver diseases, but also for alcohol-induced liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), drug-induced liver injury, viral-induced liver diseases, and cirrhosis [8,27,91,178].…”

Section: Introductionmentioning

confidence: 97%

The Gut-Liver Axis in Cholestatic Liver Diseases

Blesl

Stadlbauer

2021

Nutrients

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The gut-liver axis describes the physiological interplay between the gut and the liver and has important implications for the maintenance of health. Disruptions of this equilibrium are an important factor in the evolution and progression of many liver diseases. The composition of the gut microbiome, the gut barrier, bacterial translocation, and bile acid metabolism are the key features of this cycle. Chronic cholestatic liver diseases include primary sclerosing cholangitis, the generic term secondary sclerosing cholangitis implying the disease secondary sclerosing cholangitis in critically ill patients and primary biliary cirrhosis. Pathophysiology of these diseases is not fully understood but seems to be multifactorial. Knowledge about the alterations of the gut-liver axis influencing the pathogenesis and the outcome of these diseases has considerably increased. Therefore, this review aims to describe the function of the healthy gut-liver axis and to sum up the pathological changes in these cholestatic liver diseases. The review compromises the actual level of knowledge about the gut microbiome (including the mycobiome and the virome), the gut barrier and the consequences of increased gut permeability, the effects of bacterial translocation, and the influence of bile acid composition and pool size in chronic cholestatic liver diseases. Furthermore, therapeutic implications and future scientific objectives are outlined.

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The gut microbiome-bile acid axis in hepatocarcinogenesis

Cited by 57 publications

References 134 publications

Armillaria luteo-virens Sacc Ameliorates Dextran Sulfate Sodium Induced Colitis through Modulation of Gut Microbiota and Microbiota-Related Bile Acids

Armillaria luteo-virens Sacc Ameliorates Dextran Sulfate Sodium Induced Colitis through Modulation of Gut Microbiota and Microbiota-Related Bile Acids

Prediagnostic alterations in circulating bile acid profiles in the development of hepatocellular carcinoma

The Gut-Liver Axis in Cholestatic Liver Diseases

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