Lab Anim Res.  2019 Aug;35(2):100-106. 10.1186/s42826-019-0016-y.

Comparative study of liver injury induced by high-fat methionine- and choline-deficient diet in ICR mice originating from three different sources

  • 1College of Pharmacy, Pusan National University, Busan, South Korea.
  • 2College of Pharmacy, Brain Busan 21 Plus Program, Kyungsung University, Busan, South Korea.
  • 3Department of Clinical Laboratory Science, College of Nursing and Healthcare Science, Dong-Eui University, Busan, South Korea.
  • 4Exercise Biochemistry Laboratory, Korea National Sport University, Seoul, South Korea.
  • 5Department of Biomaterials Science, College of Natural Resources & Life Science/Life and Industry Convergence Research Institute, Pusan National University, Miryang, South Korea.
  • 6College of Veterinary Medicine, Kyungpook National University, Daegu, South Korea.


Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease worldwide. It is characterized by the accumulation of lipids without alcohol intake and often progresses to non-alcoholic steatohepatitis (NASH), liver fibrosis, and end-stage liver diseases such as cirrhosis or cancer. Although animal models have greatly contributed to the understanding of NAFLD, studies on the disease progression in humans are still limited. In this study, we used the recently reported high-fat L-methionine-defined and choline-deficient (HFMCD) diet to rapidly induce NASH and compared the responses to HFMCD in ICR mice from three different countries: Korea (supplied by the National Institute of Food and Drug Safety Evaluation), USA, and Japan during 6 weeks. Feeding HFMCD did not cause significant differences in weight gain in comparison with mice fed control diet. Relative weight of the liver increased gradually, while the relative weight of the kidneys remained unchanged. The parameters of liver injury (serum activities of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase) increased rapidly from 1 week and remained elevated for as long as 6 weeks. Histopathological analysis showed that the accumulation of hepatic lipids induced by HFMCD was prominent at 1 week after diet supplementation and increased further at 6 weeks. Inflammatory markers were significantly increased in a time-dependent manner by HFMCD. The mRNA levels of TNF-α and IL-6 were elevated approximately 15-fold relative to control diet and that of IL-1β was increased more than 20-folds at 6 week after the onset of HFMCD intake. In addition, mRNA expression of fibrosis markers such as α-SMA, TGFβ1, and Col1a1 were also significantly increased at 6 week. In summary, the responses of Korl:ICR mice by intake of HFMCD diet were similar to those of ICR mice from other sources, which suggests that Korl:ICR mice is also a useful resource to study the pathogenesis of diet-induced NAFLD.


Non-alcoholic fatty liver disease; Liver injury; High-fat L-methionine- and choline-deficient diet; ICR mouse

MeSH Terms

Alanine Transaminase
Aspartate Aminotransferases
Disease Progression
Fatty Liver
Lactic Acid
Liver Cirrhosis
Liver Diseases
Mice, Inbred ICR*
Models, Animal
Non-alcoholic Fatty Liver Disease
RNA, Messenger
Weight Gain
Alanine Transaminase
Aspartate Aminotransferases
Lactic Acid
RNA, Messenger
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