The nonshivering heat production in mitochondria-rich brown or beige adipocytes allows rodents and humans to adapt to cold stress (1). The best-characterized thermogenic effector is uncoupling protein 1 (UCP1), which dissipates energy as heat by proton transport across the mitochondrial inner membrane. Of note, there are also important UCP1-independent pathways mediating brown adipose tissue (BAT) thermogenesis (2). The discovery of significant brown and beige adipose depots in humans initiated efforts to leverage the thermogenic process as a means to increase the metabolic rate to prevent metabolic disease, such as obesity and diabetes (3). Currently, there are limited browning regimens for increased energy expenditure in humans short of cold exposure (4). In PNAS, Jiang et al. (5) investigated how the enzyme phosphoethanolamine and phosphocholine phosphatase 1 (PHOSPHO1) regulates thermogenesis in BAT, triggering changes in systemic insulin sensitivity and energy balance. PHOSPHO1 catalyzes the hydrolysis of phosphocholine (PC) to choline as well as of phosphoethanolamine (PEA) to ethanolamine and in the process, releases an inorganic phosphate group.

中文翻译：

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PHOSPHO1打破了棕色脂肪细胞的生热作用。

线粒体丰富的棕色或米色脂肪细胞中无颤动的热量产生，使啮齿动物和人类能够适应寒冷的压力（1）。最具代表性的产热效应因子是解偶联蛋白1（UCP1），它通过质子穿过线粒体内膜的运输而散发热量。值得注意的是，还有重要的不依赖UCP1的途径介导棕色脂肪组织（BAT）生热（2）。在人类中发现了明显的棕色和米色脂肪库，开始了利用产热过程的努力，以提高代谢率来预防代谢性疾病，例如肥胖症和糖尿病（3）。目前，只有很少的褐变方案可以增加人体在寒冷环境下的能量消耗（4）。在PNAS中，Jiang等人。（5）研究了磷酸乙醇胺和磷酸胆碱磷酸酶1（PHOSPHO1）酶如何调节BAT中的生热作用，从而引发系统性胰岛素敏感性和能量平衡的变化。PHOSPHO1催化磷酸胆碱（PC）水解为胆碱，以及磷酸乙醇胺（PEA）水解为乙醇胺，并在此过程中释放出无机磷酸基团。