Lipid droplet (LD) lipolysis in brown adipose tissue (BAT) is generally considered to be required for cold-induced nonshivering thermogenesis. Here, we show that mice lacking BAT Comparative Gene Identification-58 (CGI-58), a lipolytic activator essential for the stimulated LD lipolysis, have normal thermogenic capacity and are not cold sensitive. Relative to littermate controls, these animals had higher body temperatures when they were provided food during cold exposure. The increase in body temperature in the fed, cold-exposed knockout mice was associated with increased energy expenditure and with increased sympathetic innervation and browning of white adipose tissue (WAT). Mice lacking CGI-58 in both BAT and WAT were cold sensitive, but only in the fasted state. Thus, LD lipolysis in BAT is not essential for cold-induced nonshivering thermogenesisin vivo. Rather, CGI-58-dependent LD lipolysis in BAT regulates WAT thermogenesis, and our data uncover an essential role of WAT lipolysis in fueling thermogenesis during fasting.

中文翻译：

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棕色脂肪细胞中的脂解作用不是小鼠冷诱导生热所必需的

通常认为，棕色脂肪组织（BAT）中的脂滴（LD）脂解是冷诱导的非颤动热生成所必需的。在这里，我们显示缺少BAT比较基因识别-58（CGI-58）（对刺激的LD脂解必不可少的脂解性激活剂）的小鼠具有正常的生热能力，并且对寒冷不敏感。相对于同窝仔对照，这些动物在冷暴露期间提供食物时体温更高。喂食，冷暴露的基因敲除小鼠的体温升高与能量消耗增加，交感神经支配性增加和白色脂肪组织（WAT）褐变有关。BAT和WAT均缺乏CGI-58的小鼠对感冒敏感，但仅在禁食状态下。因此，BAT中的LD脂解对于体内冷诱导的非颤抖生热作用不是必需的。相反，BAT中CGI-58依赖的LD脂解调节WAT的热生成，我们的数据揭示了WAT脂解在禁食期间促进生热的重要作用。