Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8546994 | Food and Chemical Toxicology | 2018 | 8 Pages |
Abstract
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.
Keywords
NAFLDOVXTNFαMCP-1αSMAHFDTGFβALTROSASTAspartate aminotransferaseAlanine aminotransferasealpha smooth muscle actinHepatic steatosisSteatohepatitisnonalcoholic steatohepatitisEstrogenOvariectomyNonalcoholic fatty liver diseasetransforming growth factor-βtriglyceridetumor necrosis factor-αstandard dietHigh fat dietsham operationFructoseNash polymerase chain reactionPCRmonocyte chemoattractant protein-1Reactive oxygen speciesMenopause
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Authors
Tomoko Ohashi, Masaki Kato, Akihiro Yamasaki, Akifumi Kuwano, Hideo Suzuki, Motoyuki Kohjima, Yoshihiro Ogawa,