Cold exposure activates brown and brown-like adipocytes that dissipate large amounts of glucose and fatty acids via uncoupling protein 1 (UCP1) to drive non-shivering thermogenesis (NST). Evidence for the existence of these thermogenic adipocytes in adult humans gave rise to a renaissance in research on brown adipose tissue, establishing it as linchpin of energy homeostasis and metabolic health. Besides low ambient temperature, shortage or excess of food affect thermoregulation. Upon high caloric meals thermogenic adipocytes burn excess calories and maintain energy balance. In contrast, in conditions of nutrient deprivation, counter-regulatory mechanisms prevent thermogenic adipocytes from "wasting" energy substrates that need to be conserved. In this review, we discuss cell-autonomous mechanisms, metabolites, and hormones that modify NST in response to nutrient fluctuations. In particular, we focus on how thermogenic adipocytes balance thermogenesis with systemic energy homeostasis during fasting periods.

中文翻译：

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禁食和冷期间产热脂肪细胞的调节。

冷暴露激活棕色和棕色样脂肪细胞，这些脂肪细胞通过解偶联蛋白 1 (UCP1) 消散大量葡萄糖和脂肪酸，以驱动不颤抖的产热 (NST)。成年人体内存在这些产热脂肪细胞的证据引发了对棕色脂肪组织的研究的复兴，将其确立为能量稳态和代谢健康的关键。除了环境温度低外，食物短缺或过量也会影响体温调节。在高热量膳食后，产热脂肪细胞会燃烧多余的卡路里并保持能量平衡。相反，在营养缺乏的情况下，反调节机制可防止产热脂肪细胞“浪费”需要保存的能量底物。在这篇综述中，我们讨论了细胞自主机制、代谢物、和改变 NST 以响应营养波动的激素。特别是，我们关注产热脂肪细胞如何在禁食期间平衡产热与全身能量稳态。