Characterization of gut microbiomes in nonalcoholic steatohepatitis (NASH) patients: A connection between endogenous alcohol and NASH
By Lixin Zhu, S. Baker, Chelsea Gill, Wensheng Liu, Razan H. Alkhouri, R. Baker, S. Gill. Hepatology, 2013
1,603 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/51c24c526860e2c9b64a70d999c4945fa35fe9df
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- M. Pinzani
- G. Svegliati-Baroni
- E. Tsochatzis
- A. Diehl
- F. Marra
- E. Buzzetti
- Gideon M. Hirschfield
- F. Tacke
In Molecular Biology
- H. Smidt
- G. Svegliati-Baroni
- Antonio Gasbarrini
- Cesare Furlanello
- James Kinross
- Julian R. Marchesi
- F. Marra
- Loris Riccardo Lopetuso
In Pathology and Forensic Medicine
Citations in the corpus
- Blautia—a new functional genus with potential probiotic properties? (2021, background): “another study, obese children, regardless of the presence of nonalcoholic steatohepatitis, showed a higher intestinal abundance of Bacteroides and a lower abundance of Firmicutes, accompanied by reduced abundances of Blautia and Faecalibacterium.(101) A study evaluating the effect of Panax ginseng o”
- Proteobacteria: A Common Factor in Human Diseases (2017, background): “Analysis of microbiota composition in children has demonstrated a gradual increase in Proteobacteria between healthy, obese, and NASH children [40].”
- Gut microbiota profiling of pediatric nonalcoholic fatty liver disease and obese patients unveiled by an integrated meta‐omics‐based approach (2017, background): “Differences between our study and previous work likely reflect variations in environmental and dietary factors, as well as age, among the patient cohorts.((12,30)) At lower taxonomic levels, the abundance of Coriobacteriaceae, which has been linked to chronic tissue inflammation and is increased in ”
- The severity of NAFLD is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota (2016, background): “pyrosequencing) are available in the literature.((16-18)) In addition, because liver biopsy was not available in all patients to phenotype liver lesions, underdiagnosis of NASH was possible, especially in obese patients.”
- The Cirrhosis Dysbiosis Ratio defines Changes in the Gut Microbiome Associated with Cirrhosis and its Complications (2013, neutral): “Enterobacteriaceae found in most cirrhotic patients [8,9,31].”
- Enterotypes in the landscape of gut microbial community composition (2017, neutral): “Although much of the discussion emphasized the existence of three enterotypes, the original definition had made clear that they are not discrete, and that clustering is just one way to define them Reported enterotypes Three types Two types Four types Gradient D en si ty 0.0 0.4 0.8 1.2 D en si ty 1 ”
- Gut Microbiota-Derived Tryptophan Metabolites Modulate Inflammatory Response in Hepatocytes and Macrophages (2018, neutral): “As inflammation is a key secondary insult driving NASH, we investigated whether the tryptophan metabolites decreased in HFD could attenuate inflammation.”
- Lipotoxicity and the gut-liver axis in NASH pathogenesis. (2018, background): “alcohol-producing microbiota in the pathogenesis of NASH [107].”
- The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “concentrations [145].”
- The gut microbiota and host health: a new clinical frontier (2015, background): “43 Patients with NAFLD also have increased gut permeability suggesting that translocation of bacteria or microbe derived products into the portal circulation contributes to the pathogenesis.”
- Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease (2018, background): “Moreover, abundance in ethanol-producing bacteria was also observed in patients with NAFLD, indicating that this issue may lead to an oxidative stress increase and liver injury by “endogenous” production of ethanol in patients with NASH [93].”