High-fat diet stimulates the gut pathogenic microbiota and maintains hepatic injury in antibiotic-treated rats.
High-fat diet stimulates the gut pathogenic microbiota and maintains hepatic injury in antibiotic-treated rats. Cell Mol Biol (Noisy-le-grand). 2018 Jan 31;64(1):103-106 Authors: Al-Daihan S, Ben Bacha A, Al-Dbass AM, Alonazi MA, Bhat RS Abstract The gut and the liver are closely linked to each other, as changes in the gut microbiota can play a significant role in the development of many liver diseases. Gut bacteria respond rapidly to changes in diet and thus can affect the liver through their metabolites. The impact of a high lipid diet on the liver in the presence of an altered gut flora modulated by ampicillin was investigated. The study was performed on 30 male Western albino rats randomly divided into 3 groups: control (phosphate buffered saline treated), group II (ampicillin 50 mg/kg for three weeks to induce microbiota alterations and fed on standard diet) and group III (same dose of ampicillin and fed on a lipid rich diet). Stool samples were collected for qualitative determination of bacteria. Serum hepato-specific markers, in addition to Glutathione (GSH), Lipid peroxidase (MDA), Glutathione-S- transferase(GST), and vitamin C in liver tissues, were measured. Altered gut microbiota significantly increased the level of the hepato-specific marker MDA and reduced the GST, GSH and vitamin C levels. However, animals fed a lipid rich diet displayed a more significant shift in hepatic markers and antioxidants. Moreover, a new switch in composition of th...
To assess frailty, a measure of physiologic declines in multiple organ systems, in children with chronic liver disease using a novel pediatric frailty tool.
ConclusionsGiven the efficacy of rifampicin for an important sub‐group of those with cholestatic pruritus, adult patients, including those with jaundice, can be counselled that 95% of prescriptions are safe, and where hepatitis occurs, including at long latency, drug cessation appears effective.
American Journal of Gastroenterology 113, 195 (February 2018). doi:10.1038/ajg.2018.4 Author: Renuka Umashanker
Abstract Hepatitis C virus (HCV) infection is a major cause of chronic liver disease. HCV cure has been linked to improved patient outcomes. In the era of direct‐acting antivirals (DAAs), HCV cure has become the goal, as defined by sustained virological response 12 weeks (SVR12) after completion of therapy. Historically, African‐Americans have had lower SVR12 rates compared to White people in the interferon era, which had been attributed to the high prevalence of non‐CC interleukin 28B (IL28B) type. Less is known about the association between race/ethnicity and SVR12 in DAA‐treated era. The aim of the study is...
The purpose of thisworkshop is to address challenges related to clinical trial designs and drug development in Alcoholic Associated Liver Disease (AALD) and Alcoholic Hepatitis (AH) including populations to study, endpoints, and diagnostic criteria. For additional details visit https://niaaa.nih.gov/alcoholic-hepatitis-workshop-fda-niaaa-aasld
Dr David Johnson provides clinicians with an overview of the new guidelines from the American Association for the Study of Liver Diseases (AASLD) on hepatocellular carcinoma.Medscape Gastroenterology
Dr David Johnson provides clinicians with an overview of the new guidelines from the American Association for the Study of Liver Diseases (AASLD) on hepatocellular carcinoma.
This study aims to investigate the involvement of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant signaling pathway in the protection of (+)-catechin hydrate (CAT) against monocrotaline (MCT)-induced HSOS. Results of serum alanine/aspartate aminotransferases (ALT/AST) activities, total bilirubin (TBil) and bile acids (TBA) amounts, liver histological observation, scanning electron microscope evaluation and hepatic metalloproteinase-9 (MMP-9) expression all demonstrated the protection of CAT against MCT-induced HSOS in rats. CAT attenuated MCT-induced liver oxidative injury in rats and the formation of cellul...
Conclusions: The present study identified novel changes in the coding transcriptome and non-coding RNAs in the livers of NAFLD mice after metformin treatment that might shed light on the underlying mechanism by which metformin impedes the progression of NAFLD.Cell Physiol Biochem 2018;45:1487 –1505