2007 Fiscal Year Final Research Report Summary
Inputs and outputs of NPY and BDNF neurons in the hypothalamus and their implication in feeding and metabolic regulation
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 |
Section | 一般 |
Research Field |
General physiology
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Research Institution | Jichi Medical University |
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)
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Project Period (FY) |
2006 – 2007
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Keywords | feeding / glucose / NPY / BDNF / CRH / urocortin / ghrelin / leptin |
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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[Journal Article] Cell biology of insulin secretion(translation)(Editor)2007
Author(s)
Yada T, Kanazawa Y, Kasuga, M., Kashiwagi, A., Kadowaki, T., Kawamori, R., Tajima, N
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Journal Title
In Joslin' Diabetes Melitus 2nd edition
Pages: 91-119
Description
「研究成果報告書概要(欧文)」より
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