Chinese Hepatolgy ›› 2017, Vol. 22 ›› Issue (8): 700-704.

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Establishment and evaluation of a mice model for non-alcoholic fatty liver disease induced using fructose

ZHANG Cheng-liang, HE Wen-xi, XU Yan-jiao, CHANG Mu-jun, XIANG Dong, YANG Jin-yu, LIU Dong   

  1. Department of Pharmacy, Tongji Hospital Affiliated with the Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
  • Received:2017-04-20 Online:2017-08-15 Published:2020-06-16
  • Contact: LIU Dong, Email: ld2069@outlook.com

Abstract: Objective To investigate the features of the mice model for non-alcoholic fatty liver disease (NAFLD) induced using fructose.Methods C57BL/6 mice in NAFLD group were continuously fed with 30%(w/v)fructose solution for 8 weeks, while mice in normal control group were fed with distilled water. Body weight of mice in both groups was recorded. Liver was weighted and liver index was calculated after mice were sacrificed at week 2, 4, 6 and 8. Serum levels of glucose and insulin were measured and fasting insulin resistance index (FI-IR) was calculated. Indexes of lipid metabolism in serum were detected using corresponding kits. The histopathology of livers was analyzed using oil red staining and hematoxylin and eosin (HE) staining.Results Compared with those in normal control group, the body weight, liver weight and liver index of mice in NAFLD group increased obviously (P<0.05). FI-IR in NAFLD group increased continuously and was up to 4.7 times of that in normal control group at week 8 (P<0.05). Compared with normal control group, NAFLD group showed significantly higher serum levels of triglyceride, total cholesterol, low density lipoprotein and free fatty acid, while markedly lower level of high density lipoprotein (P<0.05). The histopathological results displayed small lipid droplets in liver of NAFLD group at week 2 and obvious diffused macro-vesicular lipid droplets and fat infiltration at week 8.Conclusion Thirty percent fructose diet could successfully establish NAFLD mice model, which shows similar pathological features and biochemical indices with NAFLD patients. This model can be used for the study of pathogenesis and therapy of fructose-induced NAFLD.

Key words: Fructose, Non-alcoholic fatty liver disease, Insulin resistance, Animal model