Circulating and liver tissue levels of retinol-binding protein-4 in non-alcoholic fatty liver disease

Aim:  Retinol‐binding protein‐4 (RBP4) has been proposed as a new adipokine that regulates insulin action in muscles and the liver, and contributes to the pathogenesis of insulin resistance. As non‐alcoholic fatty liver disease (NAFLD) is related to insulin resistance, we aimed to evaluate RBP4 leve...

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Published inHepatology research Vol. 39; no. 10; pp. 972 - 978
Main Authors Schina, Maria, Koskinas, John, Tiniakos, Dina, Hadziyannis, Emilia, Savvas, Savvas, Karamanos, Basil, Manesis, Emanuel, Archimandritis, Athanasios
Format Journal Article
LanguageEnglish
Published Melbourne, Australia Blackwell Publishing Asia 01.10.2009
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Summary:Aim:  Retinol‐binding protein‐4 (RBP4) has been proposed as a new adipokine that regulates insulin action in muscles and the liver, and contributes to the pathogenesis of insulin resistance. As non‐alcoholic fatty liver disease (NAFLD) is related to insulin resistance, we aimed to evaluate RBP4 levels in the serum and liver of patients with NAFLD. Methods:  Serum RBP4 was measured in 30 NAFLD patients and 30 matched healthy controls. RBP4 expression in the liver of NAFLD patients was shown by immunohistochemistry. Results:  Serum RPB4 was significantly lower in NAFLD patients compared with controls (25.15 vs 34.66 µg/mL, P < 0.001) and there was no correlation with metabolic parameters or insulin resistance. RBP4 liver tissue immunostaining was more extensive and intense in NAFLD liver compared with normal liver and the RBP4 immunohistochemical score was positively correlated with the grade of steatosis, grade of non‐alcoholic steatohepatitis activity and stage of fibrosis. Conclusions:  In NAFLD patients, serum RBP4 was significantly lower as compared with controls and did not correlate with insulin resistance. In contrast, RBP4 liver tissue expression was enhanced and correlated with NAFLD histology.
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ArticleID:HEPR534
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:1386-6346
1872-034X
DOI:10.1111/j.1872-034X.2009.00534.x