TY - JOUR
T1 - Effects of high fructose intake on liver injury progression in high fat diet induced fatty liver disease in ovariectomized female mice
AU - Ohashi, Tomoko
AU - Kato, Masaki
AU - Yamasaki, Akihiro
AU - Kuwano, Akifumi
AU - Suzuki, Hideo
AU - Kohjima, Motoyuki
AU - Ogawa, Yoshihiro
N1 - Funding Information:
This work was supported in part by a Grand-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan . This work is supported by JSPS KAKENHI Grant Number JP17K09430 .
Publisher Copyright:
© 2018 Elsevier Ltd
PY - 2018/8
Y1 - 2018/8
N2 - Epidemiology shows that the morbidity of nonalcoholic fatty liver disease (NAFLD) is increased in postmenopausal women and chronic high fructose intake induces NAFLD progression. To analyze the effects of high fructose intake on estrogen deficiency, we evaluated liver disease progression using ovariectomized mice fed with a high fat diet (HFD) for 12 weeks. Hepatic steatosis developed in all HFD groups. Fructose intake significantly increased the liver weight and serum alanine aminotransferase, which was not exacerbated by ovariectomy alone. Ovariectomy enhanced the hepatic inflammatory activity shown by tumor necrosis factor α upregulation in the groups with or without fructose intake. Both fructose intake and ovariectomy increased the hepatocytes with ballooning degeneration and hepatic macrophage infiltration and activated hepatic stellate cells. Coexistence of fructose intake and ovariectomy markedly enhanced liver cell destruction, macrophage accumulation, and progression of fibrosis. Liver damage was ameliorated by 17β-estradiol supplementation. These findings suggest that high fructose intake enhanced the progression of NAFLD in ovariectomized female mice.
AB - Epidemiology shows that the morbidity of nonalcoholic fatty liver disease (NAFLD) is increased in postmenopausal women and chronic high fructose intake induces NAFLD progression. To analyze the effects of high fructose intake on estrogen deficiency, we evaluated liver disease progression using ovariectomized mice fed with a high fat diet (HFD) for 12 weeks. Hepatic steatosis developed in all HFD groups. Fructose intake significantly increased the liver weight and serum alanine aminotransferase, which was not exacerbated by ovariectomy alone. Ovariectomy enhanced the hepatic inflammatory activity shown by tumor necrosis factor α upregulation in the groups with or without fructose intake. Both fructose intake and ovariectomy increased the hepatocytes with ballooning degeneration and hepatic macrophage infiltration and activated hepatic stellate cells. Coexistence of fructose intake and ovariectomy markedly enhanced liver cell destruction, macrophage accumulation, and progression of fibrosis. Liver damage was ameliorated by 17β-estradiol supplementation. These findings suggest that high fructose intake enhanced the progression of NAFLD in ovariectomized female mice.
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U2 - 10.1016/j.fct.2018.05.006
DO - 10.1016/j.fct.2018.05.006
M3 - Article
C2 - 29751074
AN - SCOPUS:85047068902
VL - 118
SP - 190
EP - 197
JO - Food and Chemical Toxicology
JF - Food and Chemical Toxicology
SN - 0278-6915
ER -