| Project/Area Number |
23791035
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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 |
Metabolomics
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| Research Institution | Saga University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 中枢神経 / 薬理学 / メタボリックシンドローム / GLP-1 / 糖尿病 / 内分泌 / 神経生理 / 代謝学 / 肥満 |
|---|
| Research Abstract |
GLP-1 releasing neurons show no response when gut peptides (such as GLP-1, Peptide YY and ghrelin) were applied, whereas GLP-1 releasing neurons were depolarized by leptin. CCK increased the frequency of glutamatergic synaptic inputs onto GLP-1 releasing neurons. The effects of CCK on GLP-1 releasing neurons were prevented by the pretreatment of yohimbine. Moreover, phenylephrine, a selective α1-receptor agonist, mimicked the effects of CCK on GLP-1 releasing neurons. Electrical stimulation of solitary tract showed that GLP-1 releasing neurons received direct synaptic input from vagal afferent fibers.
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