UCP1: its involvement and utility in obesity.
UCP1: its involvement and utility in obesity.
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DOI：
10.1038/ijo.2008.236
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发表时间：
2008-12
影响因子：
4.9
通讯作者：
Anunciado-Koza, R.
中科院分区：
文献类型：
--
作者：
Kozak, L. P.;Anunciado-Koza, R.
防止肥胖发展的能量平衡取决于能量消耗。尽管体力活动是消耗多余能量的主要机制，但为了保护身体免受低温而进化的生热系统是基于线粒体解偶联蛋白（UCP1）对棕色脂肪细胞中氧化磷酸化的解偶联。研究表明，通过基因操作或药物制剂上调 UCP1 可以减少肥胖并提高胰岛素敏感性。最近的证据表明棕色脂肪细胞存在两种来源，一种在胎儿发育过程中作为离散的棕色脂肪库出现，另一种在产后发育过程中作为传统白色脂肪库中的分散群体出现。后者可以通过肾上腺素能刺激来诱导，具体取决于动物的遗传背景和营养环境。了解控制这两种棕色脂肪细胞群表达的生物和环境因素有望提供新的策略，通过增强的生热作用可用于减少肥胖。
Energy balance to prevent the development of obesity is dependent on energy expenditure. Although physical activity is the dominant mechanism for dissipating excess energy, a system of thermogenesis that evolved to protect the body from hypothermia is based upon the uncoupling of oxidative phosphorylation in brown adipocytes by the mitochondrial uncoupling protein (UCP1). It has been shown that upregulation of UCP1 by genetic manipulations or pharmacological agents can reduce obesity and improve insulin sensitivity. Recent evidence has shown the existence of two sources for brown adipocytes, one appearing as discrete brown fat depots during fetal development and the other appears during post-natal development as diffuse populations in traditional white fat depots. The latter can be induced by adrenergic stimulation depending on the genetic background of the animals and the nutritional environment. Understanding the biological and environmental factors controlling the expression of these two brown adipocyte populations promises to provide new strategies by which enhanced thermogenesis can be used to reduce obesity.
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影响因子：
4.8
作者：
Brown, LJ;Koza, RA;MacDonald, MJ
通讯作者：
MacDonald, MJ
DOI：
10.1016/0006-291x(78)91036-7
发表时间：
1978-01-01
影响因子：
3.1
作者：
HIMMSHAGEN, J;DESAUTELS, M
通讯作者：
DESAUTELS, M
影响因子：
64.5
作者：
Puigserver, P;Wu, ZD;Spiegelman, BM
通讯作者：
Spiegelman, BM
影响因子：
29
作者：
Seale, Patrick;Kajimura, Shingo;Spiegelman, Bruce M.
通讯作者：
Spiegelman, Bruce M.
影响因子：
16
作者：
Barak, Y;Nelson, MC;Evans, RM
通讯作者：
Evans, RM