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Disrupted galectin‐3 causes non‐alcoholic fatty liver disease in male mice
Author(s) -
Nomoto K,
Tsuneyama K,
Abdel Aziz HO,
Takahashi H,
Murai Y,
Cui ZG,
Fujimoto M,
Kato I,
Hiraga K,
Hsu DK,
Liu FT,
Takano Y
Publication year - 2006
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2065
Subject(s) - fatty liver , endocrinology , medicine , galectin 3 , knockout mouse , peroxisome proliferator activated receptor , steatohepatitis , receptor , galectin , liver disease , triglyceride , biology , disease , immunology , cholesterol
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.