Number of the records: 1  

Analysis of Global and Absorption, Distribution, Metabolism, and Elimination Gene Expression in the Progressive Stages of Human Nonalcoholic Fatty Liver Disease

  1. 1.
    SYSNO ASEP0367248
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleAnalysis of Global and Absorption, Distribution, Metabolism, and Elimination Gene Expression in the Progressive Stages of Human Nonalcoholic Fatty Liver Disease
    Author(s) Lake, A.D. (US)
    Novák, Petr (BC-A) RID, ORCID
    Fisher, C.D. (US)
    Jackson, J.P. (US)
    Hardwick, R.N. (US)
    Billheimer, D.D. (US)
    Klimecki, W.T. (US)
    Cherrington, N.J. (US)
    Number of authors8
    Source TitleDrug Metabolism and Disposition - ISSN 0090-9556
    Roč. 39, č. 10 (2011), s. 1954-1960
    Number of pages7 s.
    Languageeng - English
    CountryUS - United States
    KeywordsSteatosis ; Steatohepatitis ; Nonalcoholic fatty liver disease
    Subject RIVEB - Genetics ; Molecular Biology
    CEZAV0Z50510513 - UMBR-M, BC-A (2005-2011)
    UT WOS000295026600023
    DOI10.1124/dmd.111.040592
    AnnotationNonalcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that range from simple fatty liver to nonalcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of human NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism, and elimination (ADME) of drugs. Differential gene expression between three clinically defined pathological groups-normal, steatosis, and NASH-was analyzed.The results suggest that uptake transporter genes are coordinately targeted for down-regulation at the global level during the pathological development of NASH and that these patients may have decreased drug uptake capacity. This coordinated regulation of uptake transporter genes is indicative of a hepatoprotective mechanism acting to prevent accumulation of toxic intermediates in disease-compromised hepatocytes.
    WorkplaceBiology Centre (since 2006)
    ContactDana Hypšová, eje@eje.cz, Tel.: 387 775 214
    Year of Publishing2012
Number of the records: 1  

  This site uses cookies to make them easier to browse. Learn more about how we use cookies.