A Novel Mouse Model for Type 2 Diabetes and Non-alcoholic Fatty Liver Disease: Spontaneous Amelioration of Diabetes by Augmented Beta Cell Mass

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  • OZE-FUKAI Aya
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine
  • FUJISAWA Tomomi
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine
  • SUGIMOTO Ken
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine
  • NOJIMA Koji
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine
  • SHINDO Nobuyasu
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine
  • SHIMOYOSHI Satomi
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine
  • YOSHIKAWA Yuki
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine
  • SATO Yoshifumi
    Department of Metabolic Medicine, Osaka University Graduate School of Medicine
  • SHIMOMURA Iichirou
    Department of Metabolic Medicine, Osaka University Graduate School of Medicine
  • IKEGAMI Hiroshi
    Department of Endocrinology, Metabolism and Diabetes, Kinki University School of Medicine
  • RAKUGI Hiromi
    Department of Geriatric Medicine, Osaka University Graduate School of Medicine

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Abstract

Given the potential for β-cells to increase their mass, glucose intolerance might be ameliorated by a compensatory increase in β-cell mass. However, it remains uncertain whether such amelioration is feasible in vivo. In this study, we investigated glucose tolerance, islet morphology, and islet gene expression of Fatty Liver Shionogi (FLS) mice, a model for non-alcoholic fatty liver disease (NAFLD). Relative to control mice, FLS mice showed an age-dependent increase in glucose intolerance up to the age of 24 weeks, leading to the development of diabetes. After this time, glucose tolerance ameliorated spontaneously and diabetes resolved by 48 week of age, associated with marked hyperinsulinemia. Islets of the FLS mice demonstrated a marked increase in β-cell mass with an increase in β-cell numbers. Islet gene expression analysis in FLS mice demonstrated no changes in gene expression of glucokinase or insulin receptor substrate 2. These data demonstrated that the 24-week-old FLS mouse is a model for type 2 diabetes with NAFLD and that the 48-week-old FLS mouse exhibits spontaneous amelioration of type 2 diabetes associated with augmented β-cell number/mass.<br>

Journal

  • Endocrine Journal

    Endocrine Journal 56 (2), 227-234, 2009

    The Japan Endocrine Society

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