| Project/Area Number |
24590333
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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 |
General pharmacology
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
AOYAMA Koji 帝京大学, 医学部, 准教授 (00420943)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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 | GTRAP3-18 / EAAC1 / 低血糖 / 食欲 / 摂食行動 / やせ / 低インスリン血症 / αMSH |
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| Outline of Final Research Achievements |
Early experiments suggested the cause of body weight loss and emaciation of GTRAP-/- to be a decrease in food intake. The level of serum MCH, AgRP or NPY, which increases appetite, was not significantly different from that of the wild type, while alpha-MSH, which inhibits appetite, was significantly increased. POMC and the receptor for alpha-MSH, MC4R, were not changed in the hypothalamus. Fasted wild type mice showed the increased activity of AMPK-alpha due to the decrease in MC4R activity in response to appetite increase. However, Fasted GTRAP-/- mice showed suppressed AMPK-alpha activity, suggesting fasting state did not lead to the decrease in MC4R activity and the increase in MSH-alpha is the primary change in GTRAP-/- mice.
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