Deficiency in galectin-3 promotes hepatic injury in CDAA diet-induced nonalcoholic fatty liver disease

Kazuhiro Nomoto*, Takeshi Nishida, Yuko Nakanishi, Makoto Fujimoto, Ichiro Takasaki, Yoshiaki Tabuchi, Koichi Tsuneyama

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

30 被引用数 (Scopus)

抄録

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 -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 (gal 3 -/-) mice and wild-type (gal 3 +/+) mice with choline-deficient L-amino-acid-defined (CDAA) diet-induced NAFLD/NASH. Hepatic injury was significantly more severe in the gal 3 - / - 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.

本文言語英語
論文番号959824
ジャーナルScientific World Journal
2012
DOI
出版ステータス出版済み - 2012

ASJC Scopus 主題領域

  • 生化学、遺伝学、分子生物学一般
  • 環境科学一般

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