| Project/Area Number |
23790276
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | チロシン脱リン酸化酵素 / TCPTP / NPY / POMC / 視床下部 / チロシン脱リン酸化酵素脱リン酸化酵素 / ARC / STAT3 / エストロジェン |
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| Research Abstract |
The purpose of the present study was to show the possible involvement of T-cell protein tyrosine phosphatase（TCPTP） via STAT3 in pro-opiomelanocortin（POMC） neurons in feeding behavior. To this end, we tried to use Cre-Lox recombination to generate POMC neurons specific deletion of TCPTP. However, we came to realize that the mouse strain which TCPTP was selectively knocked out from POMC neurons showed no behavioral abnormality andexhibited normal feeding behavior and glucose torelance. Thus we thought that another hypothalamic neuron was involved and NPY neuron was candidate. We decided to use NPY-mVenus mouse for the analysis. We also examined the regulation of the TCPTP expression by estrogen in chow and high fat fed mice. We found that the TCPTP expression was up regulated by estrogen and high fat diet. We are currently examining these results using NPY-mVenus mouse.
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