Project/Area Number |
19209035
|
Research Category |
Grant-in-Aid for Scientific Research (A)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Endocrinology
|
Research Institution | Gunma University |
Principal Investigator |
MOR Masatomo Gunma University, 大学院・医学系研究科, 教授 (80174382)
|
Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Hiroyuki 群馬大学, 大学院・医学系研究科, 講師 (20251100)
YAMADA Masanobu 群馬大学, 大学院・医学系研究科, 講師 (90261833)
OKADA Shuichi 群馬大学, 大学院・医学系研究科, 講師 (20260474)
HASHIMOTO Kohshi 群馬大学, 大学院・医学系研究科, 講師 (30396642)
INOUE Kinji 埼玉大学, 理学部, 教授 (50091963)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥49,010,000 (Direct Cost: ¥37,700,000、Indirect Cost: ¥11,310,000)
Fiscal Year 2009: ¥14,430,000 (Direct Cost: ¥11,100,000、Indirect Cost: ¥3,330,000)
Fiscal Year 2008: ¥12,480,000 (Direct Cost: ¥9,600,000、Indirect Cost: ¥2,880,000)
Fiscal Year 2007: ¥22,100,000 (Direct Cost: ¥17,000,000、Indirect Cost: ¥5,100,000)
|
Keywords | Nesfatin / 食欲調節 / 受容体 / 視床下部 / ノックアウトマウス / Nesfatin-1 / Obesity / Hypothalamus / Appetite / Receptor / Body weight |
Research Abstract |
We identified a novel receptor, G-protein coupled receptor-nesfatin (GPCRn), specific to Nesfatin-1, which is an anorexigenic molecule expressed in both the hypothalamus and peripheral tissues, including gastric and duodenal mucosa and pancreas. As expected, the hypothalamic extracts from mice deficient in the GPCRn showed a loss of specific binding of Nesfatin-1, but this specific binding was not observed in the Hella cells expressing the GPCRn. These results suggest that GPCRn may form a heterodimer with another receptors or receptor-like partners. Nesfartin-1-induced signal transduction included the pathway of Oxytocin neurons in the paraventricular nucleus and the activation of POMC and CART expression in the nucleus tract solitarius. Theses findings indicate that Nesfatin-1 is considerably involved in the regulation of obese development at the central and peripheral levels.
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