The authors of this article declared they have no conflicts of interest.
Disrupted galectin-3 causes non-alcoholic fatty liver disease in male mice
Article first published online: 6 OCT 2006
Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Journal of Pathology
Volume 210, Issue 4, pages 469–477, December 2006
How to Cite
Nomoto, K., Tsuneyama, K., Abdel Aziz, H., Takahashi, H., Murai, Y., Cui, Z.-G., Fujimoto, M., Kato, I., Hiraga, K., Hsu, D., Liu, F.-T. and Takano, Y. (2006), Disrupted galectin-3 causes non-alcoholic fatty liver disease in male mice. J. Pathol., 210: 469–477. doi: 10.1002/path.2065
- Issue published online: 9 NOV 2006
- Article first published online: 6 OCT 2006
- Manuscript Accepted: 15 AUG 2006
- Manuscript Revised: 10 AUG 2006
- Manuscript Received: 22 JUN 2006
- Japanese Ministry of Education, Science, Sports and Culture. Grant Numbers: 16790223, 18590324
- Uehara Memorial Foundation
- 21st Century COE Program in Japan
- non-alcoholic fatty liver disease (NAFLD);
- non-alcoholic steatohepatitis (NASH);
- advanced glycation end-products (AGE);
- receptor for AGE (RAGE);
- peroxisome proliferator-activated receptor γ (PPARγ)
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. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.