Ken Sugimoto    Department   Kawasaki Medical School  Kawasaki Medical School, Department of General Geriatric Medicine,    Position   Professor
Article types	原著
Language	English
Peer review	Peer reviewed
Title	A novel mouse model for type 2 diabetes and non-alcoholic fatty liver disease: spontaneous amelioration of diabetes by augmented beta cell mass.
Journal	Formal name：Endocrine journal Abbreviation：Endocr J ISSN code：13484540/09188959
Domestic / Foregin	Foregin
Volume, Issue, Page	56(2),pp.227-234
Author and coauthor	Oze-Fukai Aya, Fujisawa Tomomi, Sugimoto Ken, Nojima Koji, Shindo Nobuyasu, Shimoyoshi Satomi, Yoshikawa Yuki, Sato Yoshifumi, Shimomura Iichirou, Ikegami Hiroshi, Rakugi Hiromi
Publication date	2009
Summary	Given the potential for beta-cells to increase their mass, glucose intolerance might be ameliorated by a compensatory increase in beta-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 beta-cell mass with an increase in beta-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 beta-cell number/mass.
DOI	10.1507/endocrj.k08e-315
PMID	19088402