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Title: Deletion of the neurotrophic factor neudesin prevents diet-induced obesity by increased sympathetic activity
Authors: Ohta, Hiroya
Konishi, Morichika
Kobayashi, Yusuke
Kashio, Atsuki
Mochiyama, Takayuki
Matsumura, Shigenobu  kyouindb  KAKEN_id
Inoue, Kazuo  kyouindb  KAKEN_id  orcid (unconfirmed)
Fushiki, Tohru
Nakao, Kazuwa
Kimura, Ikuo
Itoh, Nobuyuki
Author's alias: 太田, 紘也
小西, 守周
井上, 和夫
伏木, 亨
中尾, 一和
木村, 郁夫
伊藤, 信行
Issue Date: 8-May-2015
Publisher: Nature Publishing Group
Journal title: Scientific Reports
Volume: 5
Thesis number: 10049
Abstract: Some neurotrophic factors, which are potent regulators of neuronal development and function, have recently been implicated in the control of energy balance by increasing energy expenditure. We previously identified neudesin as a novel neurotrophic factor with potential roles in the central nervous system. Although neudesin is also expressed in various peripheral tissues including adipose tissue, its physiological roles have not yet been elucidated. We found that neudesin knockout (KO) mice were resistant to high-fat diet-induced obesity and obesity-related metabolic dysfunctions. neudesin KO mice exhibited increased energy expenditure due to increased sympathetic activity, which resulted in increased heat production and fatty acid oxidation in brown adipose tissue and enhanced lipolysis in white adipose tissue. Thus, neudesin, which may be a negative regulator of sympathetic activity, could represent a novel regulator of the development of obesity and obesity-related metabolic dysfunctions.
Description: 食事性肥満の鍵因子neudesinの同定. 京都大学プレスリリース. 2015-05-08.
Rights: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
DOI(Published Version): 10.1038/srep10049
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