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

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.