Document Detail


Insulin resistance and necroinflammation drives ductular reaction and epithelial-mesenchymal transition in chronic hepatitis C.
MedLine Citation:
PMID:  20966027     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To study the mechanism(s) linking insulin resistance (IR) to hepatic fibrosis and the role of the epithelial component in tissue repair and fibrosis in chronic hepatitis C (CHC).
DESIGN: Prospective observational study.
SETTING: Tertiary care academic centre.
PATIENTS: 78 consecutive patients with CHC.
MAIN OUTCOME MEASURES: IR, calculated by the oral glucose insulin sensitivity during oral glucose tolerance test; necroinflammatory activity and fibrosis, defined according to Ishak's score; steatosis, graded as 0 (<5% of hepatocytes), 1 (5-33%), 2 (33-66%) and 3 (>66%). To evaluate the role of the epithelial component in tissue repair and fibrosis, the expansion of the ductular reaction (DR) was calculated by keratin-7 (CK7) morphometry. Nuclear expression of Snail, downregulation of E-cadherin and expression of fibroblast specific protein-1 (FSP1) and vimentin by CK7-positive cells were used as markers of epithelial-mesenchymal transition in DR elements.
RESULTS: IR, the degree of necroinflammation and expansion of the DR (stratified as reactive ductular cells (RDCs), hepatic progenitor cells and intermediate hepatobiliary cells according to morphological criteria) were all associated with the stage of fibrosis. Nuclear Snail expression, E-cadherin downregulation and vimentin upregulation were observed in RDCs. By dual immunofluorescence for CK7 and FSP1, the number of RDCs undergoing epithelial-mesenchymal transition progressively increased together with the necroinflammatory score. By multivariate analysis, total inflammation and insulin resistance were the only factors significantly predicting the presence of advanced fibrosis (Ishak score ≥3) and the expansion of RDCs.
CONCLUSION: This study indicates that IR is associated with the degree of necroinflammatory injury in CHC and contributes to hepatic fibrosis by stimulating the expansion of RDCs that express epithelial-mesenchymal transition markers.
Authors:
Gianluca Svegliati-Baroni; Graziella Faraci; Luca Fabris; Stefania Saccomanno; Massimiliano Cadamuro; Irene Pierantonelli; Luciano Trozzi; Elisabetta Bugianesi; Maria Guido; Mario Strazzabosco; Antonio Benedetti; Giulio Marchesini
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-21
Journal Detail:
Title:  Gut     Volume:  60     ISSN:  1468-3288     ISO Abbreviation:  Gut     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-14     Completed Date:  2011-01-21     Revised Date:  2011-11-24    
Medline Journal Info:
Nlm Unique ID:  2985108R     Medline TA:  Gut     Country:  England    
Other Details:
Languages:  eng     Pagination:  108-15     Citation Subset:  AIM; IM    
Affiliation:
Department of Gastroenterology, Polytechnic University of Marche, Ancona, Italy. g.svegliati@univpm.it
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MeSH Terms
Descriptor/Qualifier:
Adult
Anthropometry / methods
Disease Progression
Epithelial-Mesenchymal Transition / physiology*
Female
Glucose Tolerance Test / methods
Hepatitis C, Chronic / complications,  pathology*,  physiopathology
Humans
Insulin Resistance / physiology*
Liver / pathology*
Liver Cirrhosis / pathology,  physiopathology,  virology
Male
Middle Aged
Necrosis / physiopathology
Grant Support
ID/Acronym/Agency:
DK079005/DK/NIDDK NIH HHS; DK34989/DK/NIDDK NIH HHS; GGP09189//Telethon
Comments/Corrections
Comment In:
Gut. 2011 Jan;60(1):1-2   [PMID:  21030525 ]

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