[Activation of Kupffer cell and related signal pathway proteins in the liver of high fat and high fructose diet induced NAFLD mice]

Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2013 Oct;27(5):325-7.
[Article in Chinese]


Objective: To investigate the expression of F4/80, NF-kappaB, p-AKT, AKT in the liver of nonalcoholic fatty liver disease (NAFLD) mice. To determine the role of Kupffer cells (KCs) in the development of NASH (non-alcoholic steatohepatitis), and understand the pathogenic mechanism of NASH.

Methods: Five C3H/HeN mice fed with normal diet were served as controls, while fifteen fed with high fat, high fructose, high fat combined fructose diet respectively for 16 weeks were as NAFLD mice models. The liver inflammation and hepatic damage were examined, and the expression of F4/80, NF-Kb, p-AKT, AKT and the content of lipid in the liver were also detected.

Results: Chronic intake of high fat and 30% fructose solution caused a significant increase in hepatic steatosis in animals in comparison to water controls. Liver F4/80 and NF-kappaB were significantly higher in high fat and high fat combined fructose diet fed mice than that in controls (P < 0.01, P < 0.01), F4/80 protein were higher in high fat diet treated mice than those in fructose and high fat combined fructose groups (P < 0.01, P < 0.01). Markers of insulin resistance (e. g, hepatic phospho-AKT, AKT) were only altered in fructose-fed or high fat combined fructose animals (P < 0.01, P < 0.01).

Conclusion: High fat and fructose diet may induce NAFLD in C3H/HeN mice. Kupffer cells and signal pathway proteins were activated, and they may play key roles in the initiation and progression of NASH.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diet, High-Fat / adverse effects*
  • Fatty Liver / etiology
  • Fatty Liver / immunology*
  • Fatty Liver / metabolism
  • Female
  • Fructose / adverse effects*
  • Humans
  • Kupffer Cells / immunology*
  • Lipid Metabolism
  • Liver / immunology*
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred C3H
  • NF-kappa B / immunology
  • Non-alcoholic Fatty Liver Disease
  • Oncogene Protein v-akt / immunology
  • Signal Transduction*


  • NF-kappa B
  • Fructose
  • Oncogene Protein v-akt