Deletion of the Neurotrophic Factor neudesin Prevents Diet-induced Obesity by Increased Sympathetic Activity.
Deletion of the Neurotrophic Factor neudesin Prevents Diet-induced Obesity by Increased Sympathetic Activity.
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DOI：
10.1038/srep10049
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发表时间：
2015-05-08
影响因子：
4.6
通讯作者：
Itoh N
中科院分区：
文献类型：
--
作者：
Ohta H;Konishi M;Kobayashi Y;Kashio A;Mochiyama T;Matsumura S;Inoue K;Fushiki T;Nakao K;Kimura I;Itoh N
一些神经营养因子是神经元发育和功能的有效调节因子，最近被认为通过增加能量消耗来控制能量平衡。我们以前确定neudesin作为一种新的神经营养因子在中枢神经系统中的潜在作用。尽管neudesin也在包括脂肪组织在内的多种外周组织中表达，但其生理作用尚未阐明。我们发现neudesin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抵抗力。Neudesin KO小鼠由于交感神经活性增加而表现出增加的能量消耗，这导致棕色脂肪组织中增加的产热和脂肪酸氧化以及白色脂肪组织中增强的脂解。因此，neudesin，这可能是交感神经活性的负调节剂，可能代表肥胖症和肥胖相关的代谢功能障碍的发展的新的调节剂。
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.
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