Gut microbiota produce alcohol and contribute to NAFLD

Zhu, Lixin; Baker, Robert D.; Zhu, Rong; Baker, Susan S.

doi:10.1136/gutjnl-2016-311571

Cited by 47 publications

(35 citation statements)

References 10 publications

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“…Elevated oxidation of fatty acids [43] and endogenous alcohol [44] contribute to excessive reactive oxygen species (ROS) in the NAFLD liver. Elevated ROS levels are reflected by induction of several antioxidant enzymes such as catalase, hemoglobin and paraoxonase 1 [45–47].…”

Section: Discussionmentioning

confidence: 99%

Multi-targeting therapeutic mechanisms of the Chinese herbal medicine QHD in the treatment of non-alcoholic fatty liver disease

et al. 2017

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Beneficial effects of the Chinese herbal medicine Qushi Huayu Decoction (QHD) were observed with non-alcoholic fatty liver disease (NAFLD) patients and animal models. The impact of QHD or its active components (geniposide and chlorogenic acid, GC) on NAFLD liver transcriptome and gut microbiota was examined with NAFLD rats. Increased expression for genes required for glutathione production and decreased expression for genes required for lipid synthesis was observed in NAFLD livers treated with QHD and GC. GC treatment decreased serum LPS, which could be explained by reduced mucosal damage in the colon of GC-treated rats. Further, our data suggest an increased abundance of Treg-inducing bacteria that stimulated the Treg activity in GC treated colon, which in turn down-regulated inflammatory signals, improved gut barrier function and consequently reduced hepatic exposure to microbial products. Our study suggests that QHD simultaneously enhanced the hepatic anti-oxidative mechanism, decreased hepatic lipid synthesis, and promoted the regulatory T cell inducing microbiota in the gut.

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Section: Discussionmentioning

confidence: 99%

Multi-targeting therapeutic mechanisms of the Chinese herbal medicine QHD in the treatment of non-alcoholic fatty liver disease

et al. 2017

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“…Gut microbiota plays, indeed, a major role in the pathogenesis of many chronic liver diseases, as supported by increasing evidence. Gut microbiota is known to produce endogenous alcohol and to contribute to non-alcoholic fatty liver disease (NAFLD) 142. According to different studies, several changes in gut microbiota composition have been described in patients with NAFLD, sometimes with conflicting findings, depending on methods and features of patients and liver disease;143 144 interestingly, microbiota fingerprints of NAFLD severity have been recently identified, as increase in Bacteroides and Ruminococcus was respectively associated with non-alcoholic steatohepatitis (NASH) and with high levels of liver fibrosis 145.…”

Section: Effects Of Antibiotics On Non-communicable Disordersmentioning

confidence: 99%

Antibiotics as deep modulators of gut microbiota: between good and evil

Ianiro

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Gasbarrini

2016

Gut

534

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“…Zhu’s group examined GM composition and ethanol levels in the blood of NASH, obese, and healthy children [ 60 ]. Only a few differences were evident in the GM composition of NASH as compared with obese patients without liver disease, and included differences across phyla, families, and genera in Proteobacteria, Enterobacteriaceae, and E. coli , respectively.…”

Section: Bacterial Ethanolmentioning

confidence: 99%

Gut–Liver Axis Derangement in Non-Alcoholic Fatty Liver Disease

2017

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Non-alcoholic fatty liver disease (NAFLD) is the most frequent type of chronic liver disease in the pediatric age group, paralleling an obesity pandemic. A “multiple-hit” hypothesis has been invoked to explain its pathogenesis. The “first hit” is liver lipid accumulation in obese children with insulin resistance. In the absence of significant lifestyle modifications leading to weight loss and increased physical activity, other factors may act as “second hits” implicated in liver damage progression leading to more severe forms of inflammation and hepatic fibrosis. In this regard, the gut–liver axis (GLA) seems to play a central role. Principal players are the gut microbiota, its bacterial products, and the intestinal barrier. A derangement of GLA (namely, dysbiosis and altered intestinal permeability) may promote bacteria/bacterial product translocation into portal circulation, activation of inflammation via toll-like receptors signaling in hepatocytes, and progression from simple steatosis to non-alcoholic steato-hepatitis (NASH). Among other factors a relevant role has been attributed to the farnesoid X receptor, a nuclear transcriptional factor activated from bile acids chemically modified by gut microbiota (GM) enzymes. The individuation and elucidation of GLA derangement in NAFLD pathomechanisms is of interest at all ages and especially in pediatrics to identify new therapeutic approaches in patients recalcitrant to lifestyle changes. Specific targeting of gut microbiota via pre-/probiotic supplementation, feces transplantation, and farnesoid X receptor modulation appear promising.

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Gut microbiota produce alcohol and contribute to NAFLD

Cited by 47 publications

References 10 publications

Multi-targeting therapeutic mechanisms of the Chinese herbal medicine QHD in the treatment of non-alcoholic fatty liver disease

Multi-targeting therapeutic mechanisms of the Chinese herbal medicine QHD in the treatment of non-alcoholic fatty liver disease

Antibiotics as deep modulators of gut microbiota: between good and evil

Gut–Liver Axis Derangement in Non-Alcoholic Fatty Liver Disease

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