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Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese

机译:缺乏线粒体解偶联蛋白的小鼠对冷敏感,但不肥胖

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The mitochondrial uncoupling protein (UCP) in the mitochondrial inner membrane of mammalian brown adipose tissue generates heat by uncoupling oxidative phosphorylation. This process protects against cold and regulates energy balance. Manipulation of thermogenesis could be an effective strategy against obesity. 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 beta3-adrenergic-receptor agonist and that they are sensitive to cold, indicating that their thermoregulation is defective. However, this deficiency caused neither hyperphagia nor obesity in mice fed on either a standard or a high-fat 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.
机译: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。此过程可防止寒冷并调节能量平衡。调控生热可能是对抗肥胖的有效策略。在这里,我们通过编码UCP的基因的靶向失活来确定UCP在体重调节中的作用。我们发现,UCP缺陷型小鼠在用β3肾上腺素受体激动剂治疗后消耗的氧气更少,并且它们对寒冷敏感,表明它们的温度调节功能存在缺陷。但是,这种缺乏既不会导致以标准饮食或高脂饮食喂养的小鼠的食欲亢进也不会导致肥胖。我们建议,UCP的损失可以由UCP2(一种新发现的UCP同源物)补偿。该基因无处不在表达,并在UCP缺陷小鼠的棕色脂肪中被诱导。

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