AIM-deficient mouse fed a high-trans fat, high-cholesterol diet: a new animal model for nonalcoholic fatty liver disease

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  • Komatsu Ginga
    Laboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
  • Nonomura Toru
    Research Division Pharmacology Group, New Drug Research Center Inc., 452-1 Toiso, Eniwa-shi, Hokkaido 061-1405, Japan
  • Sasaki Mai
    Research Division Pathology Group, New Drug Research Center Inc., 452-1 Toiso, Eniwa-shi, Hokkaido 061-1405, Japan
  • Ishida Yuki
    Research Division Pharmacology Group, New Drug Research Center Inc., 452-1 Toiso, Eniwa-shi, Hokkaido 061-1405, Japan
  • Arai Satoko
    Laboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
  • Miyazaki Toru
    Laboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan AMED-CREST, Japan Agency for Medical Research and Development, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan Max Planck-The University of Tokyo Center for Integrative Inflammology, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan

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<p> Owing to changes in lifestyle, nonalcoholic fatty liver disease (NAFLD) is becoming a common form of chronic liver injury. NAFLD comprises a wide variety of disease stages, from simple steatosis to nonalcoholic steatohepatitis, which is a risk factor for the development of hepatocellular carcinoma (HCC). Because animal models for NAFLD are needed to investigate the precise pathogenesis, we aimed to establish a new mouse model employing mice deficient for apoptosis inhibitor of macrophage (AIM−/−), which exhibit accelerated lipid storage in the liver and high susceptibility to developing HCC in response to a high-fat diet (HFD). AIM−/− mice were fed the D09100301 diet, which contains 40 kcal% fat (trans fat 30 kcal%), high cholesterol (2%), and 40 kcal% carbohydrates (20 kcal% fructose), and then features of obesity and NAFLD including steatosis, inflammation, fibrosis, and HCC development were analyzed. Although a comparable grade of liver steatosis was promoted in AIM−/− mice by the D09100301 diet and the standard HFD (60 kcal% largely lard fat), significantly less lipid storage in visceral fat was observed when the mice were fed the D09100301 diet. Accelerated liver inflammation was promoted by the D09100301 diet compared with the HFD, but interestingly, HCC development was decreased in mice fed the D09100301 diet. Our findings suggest that AIM−/− mice fed the D09100301 diet exhibited a phenotype that resembled nonobese NAFLD patients and thus could be an appropriate tool to study the pathophysiology by which obesity increases the risk of HCC.</p>

収録刊行物

  • Experimental Animals

    Experimental Animals 68 (2), 147-158, 2019

    公益社団法人 日本実験動物学会

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