Project/Area Number |
17K00846
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Eating habits
|
Research Institution | Saitama Medical University (2019) The University of Tokyo (2017-2018) |
Principal Investigator |
|
Project Period (FY) |
2017-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | 糖鎖 / 代謝 / 脂質 / 非アルコール性脂肪肝炎 / 免疫難病 / 神経 / ミトコンドリア / 酸化ストレス / エネルギー / 非アルコール性脂肪性肝炎 / 炎症 / 脂質代謝 / 糖代謝 / エネルギー代謝 / シグナル伝達 / 神経科学 / 情報工学 |
Outline of Final Research Achievements |
The neural pathway via hepatic vagus nerve causes physiological lipolysis based on hepatic glycogen consumption information, in turn translating hepatic metabolism pattern as common nervous system information. As a result of working on the elucidation of this mechanism, by inhibiting the molecule X synthesized from the liver, Triglyceride in adipose tissue is preferentially used as an energy substrate of hepatocytes as compared with glycogen. Moreover the adipose tissue would be reprogrammed into brown adipose tissue. As a sum of these mechanisms, hepatic β-oxidation enhancement, inflammation suppression, and oxidative stress reduction could be triggered after the induction of RNAi on the molecule X. Based on this knowledge, PCT international patent was published.
|
Academic Significance and Societal Importance of the Research Achievements |
特許取得し開発研究を進めるとともに医薬品開発につなげていく。 さらに神経系代謝制御のメカニズムの探求し、さらに代謝を決定する細胞内器質の性状を糖鎖構造による変化から推測可能とする新たな代謝生理学へとつなげ、学術的発展に寄与できるように研究を進める。
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