Beige adipocytes can interconvert between white and brown-like states and switch between energy storage versus expenditure. Here we report that beige adipocyte plasticity is important for feeding-associated changes in energy expenditure and is coordinated by the hypothalamus and the phosphatase TCPTP. A fasting-induced and glucocorticoid-mediated induction of TCPTP, inhibited insulin signaling in AgRP/NPY neurons, repressed the browning of white fat and decreased energy expenditure. Conversely feeding reduced hypothalamic TCPTP, to increase AgRP/NPY neuronal insulin signaling, white adipose tissue browning and energy expenditure. The feeding-induced repression of hypothalamic TCPTP was defective in obesity. Mice lacking TCPTP in AgRP/NPY neurons were resistant to diet-induced obesity and had increased beige fat activity and energy expenditure. The deletion of hypothalamic TCPTP in obesity restored feeding-induced browning and increased energy expenditure to promote weight loss. Our studies define a hypothalamic switch that coordinates energy expenditure with feeding for the maintenance of energy balance.

中文翻译：

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下丘脑磷酸酶开关协调能量消耗与进食。

米色的脂肪细胞可以在白色和褐色状态之间转换，并可以在能量存储与消耗之间切换。在这里我们报告米色脂肪细胞的可塑性对于与饲料相关的能量消耗变化很重要，并且由下丘脑和磷酸酶TCPTP协调。空腹诱导和糖皮质激素介导的TCPTP抑制AgRP / NPY神经元中的胰岛素信号传导，抑制白色脂肪的褐变并减少能量消耗。相反，进食减少的下丘脑TCPTP，以增加AgRP / NPY神经元胰岛素信号传导，白色脂肪组织褐变和能量消耗。进食引起的下丘脑TCPTP抑制在肥胖症中存在缺陷。AgRP / NPY神经元中缺乏TCPTP的小鼠对饮食诱导的肥胖具有抵抗力，并且米色脂肪活性和能量消耗增加。肥胖中下丘脑TCPTP的缺失恢复了喂养引起的褐变，并增加了能量消耗以促进体重减轻。我们的研究定义了一个下丘脑开关，该开关可以协调能量消耗和进食，以维持能量平衡。