Kozak L P, Anunciado-Koza R
Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA.
Int J Obes (Lond). 2008 Dec;32 Suppl 7(Suppl 7):S32-8. doi: 10.1038/ijo.2008.236.
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.International Journal of Obesity (2008) 32, S32-S38; doi:10.1038/ijo.2008.236.
防止肥胖发生的能量平衡取决于能量消耗。虽然身体活动是消耗多余能量的主要机制，但为保护身体免受体温过低影响而进化出的产热系统是基于线粒体解偶联蛋白（UCP1）使棕色脂肪细胞中的氧化磷酸化解偶联。研究表明，通过基因操作或药物上调UCP1可减轻肥胖并改善胰岛素敏感性。最近的证据显示，棕色脂肪细胞有两个来源，一个在胎儿发育期间以离散的棕色脂肪储存形式出现，另一个在出生后发育期间以传统白色脂肪储存中的分散群体形式出现。后者可由肾上腺素能刺激诱导，这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体表达的生物学和环境因素有望提供新的策略，通过增强产热来减轻肥胖。《国际肥胖杂志》（2008年）32卷，S32 - S38；doi:10.1038/ijo.2008.236 。
