| Project/Area Number |
22500331
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | Fujita Health University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
濱田 洋司 名古屋大学, 医学(系)研究科(研究院), 准教授 (20293706)
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
|---|
| Keywords | メラニン凝集ホルモン / 阻害剤 / G蛋白共役受容体 / 摂食調節 / 神経科学 |
|---|
| Research Abstract |
We have developed a non-peptide antagonist formelanin-concentrating hormone receptor 1 (MCH1R), TPI1361-17 (TPI). TPI does not crossblood brain barrier, and the intra-peritoneal administration cause prominent anorexiceffect in mice, which suggest MCH system localize in peripheral tissues, as well as incentral nervous systems. Oral glucose load reduced MCH level in circulation. In thediet-induced obese mice, TPI reduced body weight, food intake, and improved insulinresistance. These results suggest that MCH system localize in peripheral tissues and itmay regulate energy homeostasis.
|
