TY - JOUR
T1 - Disrupted galectin-3 causes non-alcoholic fatty liver disease in male mice
AU - Nomoto, K.
AU - Tsuneyama, K.
AU - Abdel Aziz, H. O.
AU - Takahashi, H.
AU - Murai, Y.
AU - Cui, Z. G.
AU - Fujimoto, M.
AU - Kato, I.
AU - Hiraga, K.
AU - Hsu, D. K.
AU - Liu, Fu-Tong
AU - Takano, Y.
PY - 2006/12
Y1 - 2006/12
N2 - 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.
AB - 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.
KW - Advanced glycation end-products (AGE)
KW - Non-alcoholic fatty liver disease (NAFLD)
KW - Non-alcoholic steatohepatitis (NASH)
KW - Peroxisome proliferator-activated receptor γ (PPARγ)
KW - Receptor for AGE (RAGE)
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U2 - 10.1002/path.2065
DO - 10.1002/path.2065
M3 - Article
C2 - 17029217
AN - SCOPUS:33751529246
VL - 210
SP - 469
EP - 477
JO - Journal of Pathology
JF - Journal of Pathology
SN - 0022-3417
IS - 4
ER -