The maintenance of whole body energy homeostasis is critical to survival and mechanisms exist whereby an organism can adapt to its environment and the stresses placed upon it. Environmental temperature and thermogenesis are key components known to affect energy balance. However, little is known about how these processes are balanced against the overall energy balance. We show that even mild cold exposure has a significant effect on energy expenditure and UCP-1 levels which increase by 43% and 400%, respectively, when wild-type (WT) mice at thermoneutral (29 °C) were compared to mice at room temperature (22 °C) conditions. Interestingly, bone mass was lower in cold-stressed WT mice with significant reductions in femoral bone mineral content (− 19%) and bone volume (− 13%). Importantly, these cold-induced skeletal changes were absent in mice lacking NPY, one of the main controllers of energy homeostasis, highlighting the critical role of NPY in this process. However, energy expenditure was significantly greater in cold-exposed NPY null mice, indicating that suppression of non-thermogenic tissues, like bone, contributes to the adaptive responses to cold exposure. Altogether, this work identifies NPY as being crucial in coordinating energy and bone homeostasis where it suppresses energy expenditure, UCP-1 levels and lowers bone mass under conditions of cold exposure.

维持体内能量稳态对生存至关重要，并且存在一种机制，有机体可以适应环境和施加在其上的压力。环境温度和生热是已知影响能量平衡的关键因素。但是，人们对这些过程如何与整体能量平衡保持平衡知之甚少。我们显示，当温热（29°C）的野生型（WT）小鼠与温度为零的野生型（WT）小鼠相比时，即使是轻度的冷暴露也对能量消耗和UCP-1水平有显着影响，它们分别增加了43％和400％室温（22°C）条件。有趣的是，冷应激野生型小鼠的骨量较低，股骨矿物质含量（− 19％）和骨量（− 13％）显着降低。重要的，缺乏NPY（能量稳态的主要控制者之一）的小鼠缺乏这些冷诱导的骨骼变化，突显了NPY在这一过程中的关键作用。但是，在冷暴露的NPY空小鼠中，能量消耗明显更大，这表明非热源性组织（如骨骼）的抑制有助于对冷暴露的适应性反应。总而言之，这项工作确定了NPY在协调能量和骨骼稳态方面至关重要，在低温暴露条件下，NPY可以抑制能量消耗，UCP-1水平并降低骨量。有助于对冷暴露的适应性反应。总而言之，这项工作确定了NPY在协调能量和骨骼稳态方面至关重要，在低温暴露条件下，NPY可以抑制能量消耗，UCP-1水平并降低骨量。有助于对冷暴露的适应性反应。总而言之，这项工作确定了NPY在协调能量和骨骼稳态方面至关重要，在低温暴露条件下，NPY可以抑制能量消耗，UCP-1水平并降低骨量。