Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese
Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese
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DOI：
10.1038/387090a0
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发表时间：
1997-05-01
期刊：
影响因子：
64.8
通讯作者：
Kozak, LP
中科院分区：
文献类型：
--
作者：
Enerback, S;Jacobsson, A;Kozak, LP
哺乳动物棕色脂肪组织线粒体内膜中的线粒体解偶联蛋白(UCP)通过解偶联氧化磷酸化产生热量(1)。这一过程防止寒冷(2)并调节能量平衡(3)。控制生热作用可能是对抗肥胖的有效策略(4-9)。在这里，我们通过靶向失活编码UCP的基因来确定UCP在调节体重中的作用。我们发现UCP缺陷小鼠在接受治疗后消耗的氧气较少。一种β3肾上腺素能受体激动剂，它们对冷敏感，表明它们的体温调节有缺陷。然而，这种缺陷并不会导致标准饮食或高IBT饮食小鼠的过度吞噬和肥胖，我们认为UCP的丢失可以通过UCP的新发现的同源物UCP2来补偿；该基因在UCP缺陷小鼠的棕色脂肪中普遍表达并被诱导。
The mitochondrial uncoupling protein (UCP) in the mitochondrial inner membrane of mammalian brown adipose tissue generates heat by uncoupling oxidative phosphorylation(1). This process protects against cold(2) and regulates energy balance(3). Manipulation of thermogenesis could be an effective strategy against obesity(4-9). Here we determine the role of UCP in the regulation of body mass by targeted inactivation of the gene encoding it. We find that UCP-deficient mice consume less oxygen after treatment with. a beta 3-adrenergic-receptor agonist and that they are sensitive to cold, indicating that their thermo-regulation is defective. However this deficiency caused neither hyperphagia nos obesity in mice fed on either a standard or a high-ibt diet, We propose that the loss of UCP may be compensated by UCP2, a newly discovered homologue of UCP; this gene is ubiquitously expressed and is induced in the brown fat of UCP-deficient mice.