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Severe Leptin Resistance in Brown Fat-Deficient Uncoupling protein Promoter-Driven Diphtheria Toxin A Mice Despite Suppression of Hypothalamic Neuropeptide Y and Circulating Corticosterone Concentrations

机译:尽管下丘脑神经肽Y和循环皮质酮浓度的抑制,棕色脂肪缺乏的解偶联蛋白启动子驱动的白喉毒素A小鼠的严重瘦蛋白抵抗。

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摘要

Brwon adipose tissue (BAT) has the capacity for uncou- pled mitochondrial respiration and is proposed to be a key site for regulating energy expenditure in rodents. To better define the role of BAT in energy homeostasis, We previously recreated a line of transgenic mice with Deficiency of BAT (UCP promoter-driven diphtheria Toxin A transgenic mice [UCP-DTA]) mice. These mice Develop obesity that initially is due to decreased Energy expenditure and later accompanied by hyper- Phagia despite increased levels of circulating leptin.
机译:褐色脂肪组织(BAT)具有无节制的线粒体呼吸的能力,被认为是调节啮齿动物能量消耗的关键部位。为了更好地定义BAT在能量稳态中的作用,我们先前重建了一系列BAT缺乏的转基因小鼠(UCP启动子驱动的白喉毒素A转基因小鼠[UCP-DTA])小鼠。这些小鼠发展为肥胖,起初是由于能量消耗减少而导致的,尽管循环中瘦素水平升高,但伴有高食血症。

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