| Project/Area Number |
24500495
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Nagoya City University |
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Principal Investigator |
MIYOSHI ICHIRO 名古屋市立大学, 医学(系)研究科(研究院), 教授 (10183972)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMURA Tadashi 独立行政法人国立国際医療研究センター, その他部局等, 実験動物管理室長 (00333790)
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| Co-Investigator(Renkei-kenkyūsha) |
KITAMURA Hiroshi 酪農学園大学, 獣医学部, 教授 (80312403)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 疾患モデル / スフィンゴ糖脂質 / 血糖調節 / 遺伝子組換えマウス / 脂肪組織 |
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| Outline of Final Research Achievements |
We attempted to elucidate the involvement of the glycosphingolipids in the blood sugar level regulation by comparison analysis of the pathological condition of glucosylceramide synthase(Ugcg) gene-manipulated mice fed with high-fat diet. The body weight gain was drastic in KoHe mice expressing lower Ugcg activity, but retarded in TgM mice expressing higher Ugcg activity. KoHe showed insulin resistance and hyperinsulinemia with hypertrophy and hyperplasia of pancreatic islet and severe accumulation of lipid and glycogen in liver. On the contrary, apparent impairment in insulin secretion was demonstrated in TgM. KoHe and TgM is useful model for obese diabetes and non-obese diabetes, respectively.
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