In eukaryotic cells, the mammalian target of rapamycin complex 1 (sometimes referred to as the mechanistic target of rapamycin complex 1; mTORC1) orchestrates cellular metabolism in response to environmental energy availability. As a result, at the organismal level, mTORC1 signalling regulates the intake, storage and use of energy by acting as a hub for the actions of nutrients and hormones, such as leptin and insulin, in different cell types. It is therefore unsurprising that deregulated mTORC1 signalling is associated with obesity. Strategies that increase energy expenditure offer therapeutic promise for the treatment of obesity. Here we review current evidence illustrating the critical role of mTORC1 signalling in the regulation of energy expenditure and adaptive thermogenesis through its various effects in neuronal circuits, adipose tissue and skeletal muscle. Understanding how mTORC1 signalling in one organ and cell type affects responses in other organs and cell types could be key to developing better, safer treatments targeting this pathway in obesity.

在真核细胞中，雷帕霉素复合物 1 的哺乳动物靶标（有时称为雷帕霉素复合物 1 的机械靶标；mTORC1）根据环境能量可用性协调细胞代谢。因此，在生物体水平上，mTORC1 信号传导通过充当不同细胞类型中营养素和激素（例如瘦素和胰岛素）作用的枢纽来调节能量的摄入、储存和使用。因此，mTORC1 信号传导失调与肥胖相关也就不足为奇了。增加能量消耗的策略为肥胖症的治疗提供了治疗希望。在这里，我们回顾了当前的证据，说明 mTORC1 信号传导通过其对神经元回路、脂肪组织和骨骼肌的各种影响，在能量消耗和适应性生热调节中发挥着关键作用。了解一种器官和细胞类型中的 mTORC1 信号传导如何影响其他器官和细胞类型的反应可能是开发针对肥胖这一途径的更好、更安全治疗方法的关键。