| Project/Area Number |
16K09767
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Metabolomics
|
|---|
| Research Institution | Kanazawa Medical University |
|---|
Principal Investigator |
TANIDA Mamoru 金沢医科大学, 医学部, 准教授 (70512309)
|
|---|
| Research Collaborator |
GOTOH Hitoshi
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 自律神経 / 視床下部 / 延髄 / エネルギー代謝 / 脂肪組織 / 摂食調節 / nesfatin-1 / 肥満 / 延髄カテコラミンニューロン / 白色脂肪 / 神経ペプチド / シグナル伝達 |
|---|
| Outline of Final Research Achievements |
It is well known that metabolic syndrome such as obesity, hypertension or diabetes, is major health issue in the world. To contribute to establishment of new treatment to the metabolic syndrome, we focus to nefatin-1, appetite suppressor in the brain, and examined central mechanism of nesfatin-1 actions on sympathetic outflow to the adipose tissue. Here, we newly found central pathway that nesfatin-1 caused sympathetic activation in the white adipose tissue through the hypothalamic ERK signal and the medullary catecholaminergic signal. Thus, it seems that present new data may contribute to new preventive method and treatment to the obesity.
|
| Academic Significance and Societal Importance of the Research Achievements |
本研究で新たに得られた成果は、自律神経を介する摂食とエネルギー代謝に関する脳内調節機構を新たに見出していることである。このことから、本研究の成果は、自律神経系調節に関する基礎医学系分野への貢献のみならず、生活習慣病の新規創薬開発や抗肥満戦略におけるnesfatin-1作用の有効性を追求する研究分野にも大きな影響をもたらし、健康寿命の遅延を招く生活習慣病予防・治療に貢献するものである。
|
