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神经营养因子neudesin的缺失通过增强交感神经活动预防饮食诱导的肥胖。

Deletion of the Neurotrophic Factor neudesin Prevents Diet-induced Obesity by Increased Sympathetic Activity.

作者信息

Ohta Hiroya, Konishi Morichika, Kobayashi Yusuke, Kashio Atsuki, Mochiyama Takayuki, Matsumura Shigenobu, Inoue Kazuo, Fushiki Tohru, Nakao Kazuwa, Kimura Ikuo, Itoh Nobuyuki

机构信息

Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto, Japan.

1] Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto, Japan [2] Department of Microbial Chemistry, Kobe Pharmaceutical University, Kobe, Japan.

出版信息

Sci Rep. 2015 May 8;5:10049. doi: 10.1038/srep10049.

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.

摘要

一些神经营养因子是神经元发育和功能的有效调节因子,最近有研究表明它们通过增加能量消耗来控制能量平衡。我们之前鉴定出神经趋化素是一种在中枢神经系统中具有潜在作用的新型神经营养因子。尽管神经趋化素也在包括脂肪组织在内的各种外周组织中表达,但其生理作用尚未阐明。我们发现神经趋化素基因敲除(KO)小鼠对高脂饮食诱导的肥胖和肥胖相关的代谢功能障碍具有抗性。神经趋化素基因敲除小鼠由于交感神经活动增加而导致能量消耗增加,这导致棕色脂肪组织中产热增加和脂肪酸氧化增加,白色脂肪组织中脂解增强。因此,神经趋化素可能是交感神经活动的负调节因子,它可能代表了肥胖及肥胖相关代谢功能障碍发生发展的一种新型调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/681d/4424804/8ea557437f0b/srep10049-f1.jpg

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