Study [NASH] study / subjects / design / samples / assays

Basic properties of your study This page shows the basic information about your study, as well as information on the authorizations.

Publications

Contacts

  • Bouwman, Jildau
    Data Submission

Authorization

Public Design
Yes
Readers
jildau.bouwman
annelies.dijk
ferry.jagers
suzan.wopereis
everton.lima
joost.westerhout
tno.user
tim.vandenbroek
lars.verschuren
marjan.vanerk
pol.grootswagers
willem.vandenbrink
femke.hoevenaars
wouter.zirkzee
paula.santos
lodewic.vantwillert
martien.caspers
eugene.vansomeren
ben.vanommen
heleen.deweerd
annemarie.prins
remon.dulos
herman.wietmarschen
peter.wielinga
andre.boorsma
Writers
Study title
Adipose Tissue Dysfunction Signals Progression of Hepatic Steatosis Towards Nonalcoholic Steatohepatitis in C57Bl/6 Mice
Template
Intervention/Observation study
title
Adipose Tissue Dysfunction Signals Progression of Hepatic Steatosis Towards Nonalcoholic Steatohepatitis in C57Bl/6 Mice
description
OBJECTIVE—Nonalcoholic fatty liver disease (NAFLD) is linked to obesity and diabetes, suggesting an important role of adipose tissue in the pathogenesis of NAFLD. Here, we aimed to investigate the interaction between adipose tissue and liver in NAFLD and identify potential early plasma markers that predict nonalcoholic steatohepatitis (NASH). RESEARCH DESIGN AND METHODS—C57Bl/6 mice were chronically fed a high-fat diet to induce NAFLD and compared with mice fed a low-fat diet. Extensive histological and phenotypical analyses coupled with a time course study of plasma proteins using multiplex assay were performed. RESULTS—Mice exhibited pronounced heterogeneity in liver histological scoring, leading to classification into four subgroups: low-fat low (LFL) responders displaying normal liver morphology, low-fat high (LFH) responders showing benign hepatic steatosis, high-fat low (HFL) responders displaying pre-NASH with macrovesicular lipid droplets, and high fat high (HFH) responders exhibiting overt NASH characterized by ballooning of hepatocytes, presence of Mallory bodies, and activated inflammatory cells. Compared with HFL responders, HFH mice gained weight more rapidly and exhibited adipose tissue dysfunction characterized by decreased final fat mass, enhanced macrophage infiltration and inflammation, and adipose tissue remodeling. Plasma haptoglobin, IL-1, TIMP-1, adiponectin, and leptin were significantly changed in HFH mice. Multivariate analysis indicated that in addition to leptin, plasma CRP, haptoglobin, eotaxin, and MIP-1 early in the intervention were positively associated with liver triglycerides. Intermediate prognostic markers of liver triglycerides included IL-18, IL-1, MIP-1, and MIP-2, whereas insulin, TIMP-1, granulocyte chemotactic protein 2, and myeloperoxidase emerged as late markers. CONCLUSIONS—Our data support the existence of a tight relationship between adipose tissue dysfunction and NASH pathogenesis and point to several novel potential predictive biomarkers for NASH.
code
NASH
startDate
2005-01-03 00:00:00.0
Study type
Animal Intervention
Objectives
—Nonalcoholic fatty liver disease (NAFLD) is linked to obesity and diabetes, suggesting an important role of adipose tissue in the pathogenesis of NAFLD. Here, we aimed to investigate the interaction between adipose tissue and liver in NAFLD and identify potential early plasma markers that predict nonalcoholic steatohepatitis (NASH).
Institute
Wageningen University
Consortium
not defined

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