The contribution of brown and BRITE adipocytes to adaptive thermogenesis and body weight regulation

哺乳动物利用褐色脂肪组织进行非寒颤产热（NST），通过将呼吸与ATP合成分离。这种产热模式是由棕色脂肪细胞中的线粒体解偶联蛋白1 （UCP1）催化的。ucp1介导的NST是冷适应中必不可少的适应性产热的重要组成部分，也可能有助于能量平衡调节。除了依赖ucp1的NST外，在骨骼肌和白色脂肪组织中也可以找到其他不依赖ucp1的适应性产热机制。白色脂肪组织中的棕色脂肪细胞，被称为BRITE（褐色中白）或Beige脂肪细胞，能够依赖ucp1和独立的NST。在这个项目中，将研究NST的发展和潜在的分子机制，以及这些机制对能量平衡调节的贡献。通过使用细胞特异性启动子对ucp1基因进行组织特异性删除，将在体内分析BRITE脂肪细胞的产热能力。

Mammals employ brown adipose tissue for nonshivering thermogenesis (NST) by uncoupling respiration from the ATP synthesis. This mode of thermogenesis is catalysed by the mitochondrial uncoupling protein 1 (UCP1) in brown adipocytes. UCP1-mediated NST is a substantial component of adaptive thermogenesis essential in cold adaptation and may also contribute to energy balance regulation. Besides UCP1-dependent NST, alternative UCP1-independent mechanisms of adaptive thermogenesis can be recruited in skeletal muscle and white adipose tissue. Brown adipocytes in white adipose tissue, known as BRITE (brown-in-white) or Beige adipocytes, are capable of UCP1-dependent and independent NST. In this project the development of NST and the underlying molecular mechanisms as well as the contribution of these mechanisms to energy balance regulation will be investigated. By tissue specific deletion of the Ucp1-gene using a cell-specific promoter the thermogenic capacity of BRITE adipocytes will be analysed in vivo.