| Project/Area Number |
18390065
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Jichi Medical University |
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Principal Investigator |
YADA Toshihiko Jichi Medical University, School of Medicine, Professor (60166527)
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| Co-Investigator(Kenkyū-buntansha) |
NAKATA Masanori Jichi Medical University, School of Medicine, Associate Professor (10305120)
DEZAKI Katsuya Jichi Medical University, School of Medicine, Assistant Professor (90337329)
FUJIWARA Ken Jichi Medical University, School of Medicine, Research Associate (00382945)
TORIYA Masako Jichi Medical University, School of Medicine, 21st Century COE Program, Post-doctral fellow (90420819)
MAEJIMA Yuko Jichi Medical University, School of Medicine, Research Associate (40438669)
河野 大輔 自治医科大学, 医学部, 研究生 (10382904)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥14,810,000 (Direct Cost: ¥13,100,000、Indirect Cost: ¥1,710,000)
Fiscal Year 2007: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
Fiscal Year 2006: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | feeding / glucose / NPY / BDNF / CRH / urocortin / ghrelin / leptin / 弓状核 / NPYニューロン / Ca^<2+> / レぷちん / 室傍核 |
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| Research Abstract |
We analyzed the inputs and outputs of neuropeptide Y (NPY) neurons and brain-derived neurotrophic factor (BDNF) neurons. NPY neurons in the hypothalamic arcuate : nucleus (ARC) were activated by ghrelin and inhibited by leptin. Leptin, via PI3 kinase and PDE3 signaling pathway, counteracted the action of ghrelin in NPY neurons. The integration of the two hormones determined the activity of NPY neurons and the feeding behavior. GK rats, a model of type 2 diabetes, showed young-adult specific hyperphagia, which was caused by elevated expression of NPY mRNA in the ARC, suggesting the pathophysiological role of the ARC NPY neurons.
Central injection of BDNF increased expression of corticotropin-releasing hormone (CRH) and urocortin in the paraventricular nucleus (PVN), and thereby inhibited feeding and enhanced energy expenditure via CRH-R2 receptors. A new anorectic peptide, nesfatin-1, was abundant in PVN and colocalized with CRH, suggesting that nesfatin-1 could serve as a regulator of BDNF-CRH system.
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