Disrupted galectin-3 causes non-alcoholic fatty liver disease in male mice

K. Nomoto, K. Tsuneyama, H. O. Abdel Aziz, H. Takahashi, Y. Murai, Z. G. Cui, M. Fujimoto, I. Kato, K. Hiraga, D. K. Hsu, Fu-Tong Liu, Y. Takano

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

Galectin-3, a β-galactoside-binding animal lectin, is a multifunctional protein. Previous studies have suggested that galectin-3 may play an important role in inflammatory responses. Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as a liver condition that may progress to end-stage liver disease and based on the known functions of galectin-3, it was hypothesized that galectin-3 might play a role in the development of NAFLD. Thus, this study investigated the role of galectin-3 in NAFLD by comparing galectin-3 knockout (gal3-/-) mice and wild-type (gal3+/+) mice. The livers of gal3-/- male mice at 6 months of age histologically displayed mild to severe fatty change. The liver weight per body weight ratio, serum alanine aminotransferase levels, liver triglyceride levels, and liver lipid peroxide in gal3-/- mice were significantly increased compared with those in gal3+/+ mice. Furthermore, the hepatic protein levels of advanced glycation end-products (AGE), receptor for AGE (RAGE), and peroxisome proliferator-activated receptor γ (PPARγ) were increased in gal3-/- mice relative to gal3+/+ mice. In conclusion, this study suggests that the absence of gal3 can cause clinico-pathological features in male mice similar to those of NAFLD.

Original languageEnglish (US)
Pages (from-to)469-477
Number of pages9
JournalJournal of Pathology
Volume210
Issue number4
DOIs
StatePublished - Dec 2006

Keywords

  • Advanced glycation end-products (AGE)
  • Non-alcoholic fatty liver disease (NAFLD)
  • Non-alcoholic steatohepatitis (NASH)
  • Peroxisome proliferator-activated receptor γ (PPARγ)
  • Receptor for AGE (RAGE)

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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