Lipid Droplets in Brown Adipose Tissue Are Dispensable for Cold-Induced Thermogenesis.

Brown adipocytes store metabolic energy as triglycerides (TGs) in lipid droplets (LDs). Fatty acids released from brown adipocyte LDs by lipolysis are thought to activate and fuel UCP1-mediated thermogenesis. Here, we test this hypothesis by preventing fatty acid storage in murine brown adipocytes through brown adipose tissue (BAT)-specific deletions of the TG synthesis enzymes DGAT1 and DGAT2 (BA-DGAT KO). Despite the absence of TGs in brown adipocytes, BAT is functional, and BA-DGAT-KO mice maintain euthermia during acute or chronic cold exposure. As apparent adaptations to the lack of TG, brown adipocytes of BA-DGAT-KO mice appear to use circulating glucose and fatty acids, and stored glycogen, to fuel thermogenesis. Moreover, BA-DGAT-KO mice are resistant to diet-induced glucose intolerance, likely because of increased glucose disposal by BAT. We conclude that TGs in BAT are dispensable for its contribution to cold-induced thermogenesis, at least when other fuel sources are available. Chitraju et al. show that mice lacking triglycerides and lipid droplets in brown adipocytes maintain euthermia during acute or chronic cold exposure by using circulating glucose and fatty acids and stored glycogen to fuel thermogenesis.

棕色脂肪细胞将代谢能量以甘油三酯（TGs）的形式储存在脂滴（LDs）中。通过脂解作用从棕色脂肪细胞脂滴中释放的脂肪酸被认为可激活并为解偶联蛋白1（UCP1）介导的产热提供能量。在此，我们通过在棕色脂肪组织（BAT）中特异性敲除甘油三酯合成酶二酰基甘油酰基转移酶1（DGAT1）和二酰基甘油酰基转移酶2（DGAT2）（BA - DGAT基因敲除）来阻止脂肪酸在小鼠棕色脂肪细胞中的储存，以此检验这一假说。尽管棕色脂肪细胞中没有甘油三酯，但棕色脂肪组织仍有功能，并且BA - DGAT基因敲除小鼠在急性或慢性寒冷暴露期间能维持正常体温。作为对缺乏甘油三酯的明显适应性变化，BA - DGAT基因敲除小鼠的棕色脂肪细胞似乎利用循环中的葡萄糖和脂肪酸以及储存的糖原为产热提供能量。此外，BA - DGAT基因敲除小鼠对饮食诱导的葡萄糖耐受不良具有抵抗力，这可能是因为棕色脂肪组织对葡萄糖的处理增加。我们得出结论，棕色脂肪组织中的甘油三酯对于其在寒冷诱导的产热中的作用并非不可或缺，至少在有其他能量来源时是这样。 奇特拉朱（Chitraju）等人表明，棕色脂肪细胞中缺乏甘油三酯和脂滴的小鼠在急性或慢性寒冷暴露期间，通过利用循环中的葡萄糖和脂肪酸以及储存的糖原为产热提供能量，从而维持正常体温。