Disrupted galectin-3 causes non-alcoholic fatty liver disease in male mice |
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Authors: | Nomoto K Tsuneyama K Abdel Aziz H O Takahashi H Murai Y Cui Z-G Fujimoto M Kato I Hiraga K Hsu D K Liu F-T Takano Y |
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Institution: | Department of Pathology, Faculty of Medicine, University of Toyama, Toyama, Japan. |
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Abstract: | Galectin-3, a beta-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 gamma (PPARgamma) 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. |
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Keywords: | 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) |
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