title: Gene expression patterns in hepatic tissue and visceral adipose tissue of patients with non-alcoholic fatty liver disease.
abstract: BACKGROUND
  Non-alcoholic fatty liver disease (NAFLD) and its progressive form, non-alcoholic steatohepatitis (NASH), are among the least understood metabolic consequences of obesity. Increasingly, omental adipose tissue is recognized as a biologically active organ in the pathogenesis of NAFLD. Differences in transcriptional regulation in omental adipose tissue and liver tissue may provide important insights into the pathogenesis of NAFLD and its progression.
  
  
  METHODS
  Transcriptional profiles were obtained for liver and visceral adipose specimens of morbidly obese patients undergoing bariatric surgery. Functional analyses with the Ingenuity Pathways Knowledge Base (IPKB) and IPA 4.0 software identified genes that potentially play hepatoprotective roles as well as those potentially involved in the pathogenesis of NASH. TNFalpha and IL6 were measured in the serum samples.
  
  
  RESULTS
  Tissue from patients with NASH showed prominent adipose-specific deregulation of genes related to inflammation and the immune system. A number of liver and adipose-specific functional networks, including those centered at TNFalpha, JUN/JUNB, and IFNgamma were highlighted as related to the NASH pathogenesis. The results also showed compensatory increases in hepatic detoxification enzymes and decreases in the gene network controlled by transcription factor COUP-TFII.
  
  
  CONCLUSIONS
  Our findings support the hypothesis that adipocyte secretion plays an important role in the development of NAFLD.
authors.affiliation: Center for Liver Diseases, Inova Fairfax Hospital, Fairfax, VA 22042, USA.
authors.forename: Ancha
authors.initials: A
authors.lastname: Baranova
authors.forename: Karen
authors.initials: K
authors.lastname: Schlauch
authors.forename: Hazem
authors.initials: H
authors.lastname: Elariny
authors.forename: Mohammed
authors.initials: M
authors.lastname: Jarrar
authors.forename: Chase
authors.initials: C
authors.lastname: Bennett
authors.forename: Clare
authors.initials: C
authors.lastname: Nugent
authors.forename: Shobha J
authors.initials: SJ
authors.lastname: Gowder
authors.forename: Zahra
authors.initials: Z
authors.lastname: Younoszai
authors.forename: Rochelle
authors.initials: R
authors.lastname: Collantes
authors.forename: Vikas
authors.initials: V
authors.lastname: Chandhoke
authors.forename: Zobair M
authors.initials: ZM
authors.lastname: Younossi
mesh_terms: D017667:Adipocytes / Q000502:physiology*; D000328:Adult; D004797:Enzyme-Linked Immunosorbent Assay; D005234:Fatty Liver / Q000235:genetics* / Q000503:physiopathology / Q000517:prevention & control; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000502:physiology*; D016758:Genes, jun / Q000235:genetics; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics / Q000502:physiology; D015850:Interleukin-6 / Q000097:blood; D050152:Intra-Abdominal Fat / Q000166:cytology* / Q000378:metabolism; D020738:Leptin / Q000378:metabolism; D008099:Liver / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000235:genetics / Q000378:metabolism; D040081:Protein Array Analysis; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma