| Project/Area Number |
23659385
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General internal medicine (including Psychosomatic medicine)
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KOMORI Tadasuke 和歌山県立医科大学, 医学部, 助教 (90433359)
FURUTA Hiroto 和歌山県立医科大学, 医学部, 講師 (90238684)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ストレス / 絶食 / 転写因子 / モデルマウス / 神経性食思不振症 / 摂食調節 / 視床下部 |
|---|
| Research Abstract |
In a hypothalamic neuronal cell line, GT1-7 cells, AF5q31 specifically increased the expression of AMPKα2 subunit at the transcriptional level. In addition, AF5q31activated AMPK signal pathway by a novel mechanism, which is independent of AMPKαphosphorylation. AF5q31+/-mice exhibited the disturbance of both HPA axis and glucose metabolism, which are observed in the patients with anorexia nervosa. Thus, AF5q31+/-mice provide a unique mouse model of anorexia nervosa.
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