期刊
SCIENTIFIC WORLD JOURNAL
卷 -, 期 -, 页码 1-9出版社
HINDAWI PUBLISHING CORPORATION
DOI: 10.1100/2012/959824
关键词
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资金
- Japanese Ministry of Education, Science, Sports and Culture [16790223, 18590324]
- Uehara Memorial Foundation
- 21st century COE program in Japan
- Grants-in-Aid for Scientific Research [16790223, 18590324] Funding Source: KAKEN
Nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a condition in which excess fat accumulates in hepatocytes. Nonalcoholic steatohepatitis (NASH), a severe form of NAFLD in which inflammation and fibrosis in the liver are noted, may eventually progress to end-stage liver disease. Galectin-3, a beta-galactoside-binding animal lectin, is a multifunctional protein. This protein is involved in inflammatory responses and carcinogenesis. We investigated whether galectin-3 is involved in the development of NASH by comparing galectin-3 knockout (gal3(-/-)) mice and wild-type (gal3(+/+)) mice with choline-deficient L-amino-acid-defined (CDAA) diet-induced NAFLD/NASH. Hepatic injury was significantly more severe in the gal3(-/-) male mice, as compared to the gal(3+/+) mice. Data generated by microarray analysis of gene expression suggested that galectin-3 deficiency causes alterations in the expression of various genes associated with carcinogenesis and lipid metabolism. Through canonical pathway analysis, involvement of PDGF and IL-6 signaling pathways was suggested in galectin-3 deficiency. Significant increase of CD14, Fos, and Jun, those that were related to lipopolysaccharide-mediated signaling, was candidate to promote hepatocellular damages in galectin-3 deficiency. In conclusion, galectin-3 deficiency in CDAA diet promotes NAFLD features. It may be caused by alterations in the expression profiles of various hepatic genes including lipopolysaccharide-mediated inflammation.
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