Abstract
Non-alcoholic fatty liver disease (NAFLD) is a complex disease ranging from steatosis to non-alcoholic steatohepatitis (NASH). Galectin-3 (Gal-3), which is a β-galactoside binding protein, has been associated with liver fibrosis, but its role in NAFLD remains elusive. We investigated the expression of Gal-3 in liver resident cells and its potential association with liver damage in 40 children with biopsy-proven NAFLD. We found that several liver cells expressed Gal-3. The number of total Gal-3 positive cells decreased with the severity of disease and the cells were correlated with the presence of steatosis and the diagnosis of NASH. CD68 macrophages expressed Gal-3 but the number CD68/Gal-3 positive cells was significantly reduced in patients diagnosed with steatosis and NASH. Triple CD68/CD206/Gal-3, which represented the subpopulation of M2 macrophages, were mainly present in patients without NASH, and clearly reduced in patients with steatosis and NASH. On the contrary, the number of α-smooth muscle actin (SMA)/Gal-3 positive cells increased with the severity of fibrosis in children with NAFLD. Our data demonstrated that the number of Gal-3 positive cells was associated with tissue damage in different ways, which suggests a dual role of this protein in the pathogenesis of pediatric NAFLD, even if the role of Gal-3 deserves further studies.
Highlights
Non-alcoholic fatty liver disease (NAFLD), which is currently recognized as the most frequent cause of chronic liver disease worldwide, is a fatty liver condition occurring in the absence of alcohol consumption mainly associated with central obesity [1].NAFLD comprises a large spectrum of histopathologic feature, which ranges from variable degrees of abnormal fat accumulation into hepatocytes to hepatic inflammation and eventually fibrosis [2]
The Number of Gal-3 Positive Cells Correlates with the Severity of Disease in Children with NAFLD
These discordant findings open questions on the real role of Gal-3GinalN-3AhFaLs Dal.so been indicated as a pro-inflammatory mediator, which is largely involved with macrGopahl-a3gheaasctaivlsaotiboeneanndinmdiicgartaetdionas[1a1]p. rIon-itnhfelaamnamlgaetsoircyacmeteadmiaintoorp, hwenhiacdhmisinliasrtgraetliyoninevxoplevreidmewnittahl macrophage activation and migration [11]
Summary
Non-alcoholic fatty liver disease (NAFLD), which is currently recognized as the most frequent cause of chronic liver disease worldwide, is a fatty liver condition occurring in the absence of alcohol consumption mainly associated with central obesity [1]. Experimental diet-induced NAFLD was more severe in the absence of Gal-3 with significant liver damages. These mice that were submitted to a high fat diet developed significant visceral adiposity, diabetes, and liver steatosis correlated with a reduced number of myeloid dendritic cells and proinflammatory macrophages [18,19]. During choline-deficient L-amino-acid-defined (CDAA) diet-induced NAFLD, Lgals3−/− mice showed drastic hepatocellular injuries and pattern of gene expression associated with carcinogenesis and lipid metabolism [20]. We investigated whether Gal-3 expression in liver cells may be associated with tissue damage in children with biopsy-proven NAFLD
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
