The analysis of neudesin, a secretory molecule, for developing an anti-obesity drug
Project/Area Number |
15K18863
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Biological pharmacy
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Research Institution | Nagoya University (2016) Kobe Pharmaceutical University (2015) |
Principal Investigator |
Ohta Hiroya 名古屋大学, 環境医学研究所, 助教 (40638988)
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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Keywords | neudesin / ノルアドレナリン / 交感神経系 / 脂肪組織 |
Outline of Final Research Achievements |
We previously reported that the neudesin KO mice were resistant to diet-induced obesity. neudesin KO mice showed increased energy expenditure due to increased sympathetic nervous activity. We newly found that recombinant neudesin protein acted on differentiated PC12 cells to suppress tyrosine hydroxylase (Th), which is a rate-limiting enzyme of noradrenaline synthesis. We also found that neudesin directly acted on white adipocytes to suppress adrenaergic stimuli on adipocytes.
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Report
(3 results)
Research Products
(12 results)
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[Journal Article] Deletion of Neurotrophic Factor neudesin Prevents Diet-induced Obesity by Increased Sympathetic Activity2015
Author(s)
Hiroya Ohta, Morichika Konishi, Yusuke Kobayashi, Atsuki Kashio, Takayuki Mochiyama, Shigenobu Matsumura, Kazuo Inoue, Tohru Fushiki, Kazuwa Nakao, Ikuo Kimura, Nobuyuki Itoh
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Journal Title
Scientific Reports
Volume: 印刷中
Issue: 1
Pages: 10049-10049
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Presentation] 分泌性因子neudesinの遺伝子欠損マウスは交感神経活性の亢進により食餌誘導性肥満に耐性示す2015
Author(s)
太田紘也, 小西守周, 橋本大嗣, 樫尾篤樹, 持山喬之, 松村成暢, 井上和生, 伏木亨, 中山喜明, 中尾一和, 木村郁夫, 伊藤信行
Organizer
第38回日本分子生物学会年会
Place of Presentation
神戸
Year and Date
2015-12-03
Related Report
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