Web Map For Collection 中文 English
 
Home About us Organization Principal Investigators Research Education& Training Academic activities Facilities Careers Downloads Contact us
Location:Home - Research - Articles
Articles
Zhou Z, Toh SY, Chen A, Guo K, Ng CP, Ponniah S, Lin SC, Hong W, and Li P. CIDE-A deficient mice exhibit lean phenotype and are obesity resistant. NATURE GENETICS 35: 49-56, 2003
Time:2011-11-17Author:李蓬KeyWord:

Abstract
The thermogenic activity of brown adipose tissue (BAT), important for adaptive thermogenesis and energy expenditure, is mediated by the mitochondrial uncoupling protein1 (Ucp1) that uncouples ATP generation and dissipates the energy as heat. We show here that Cidea, a protein of unknown function sharing sequence similarity with the N-terminal region of DNA fragmentation factors Dffb and Dffa, is expressed at high levels in BAT. Cidea-null mice had higher metabolic rate, lipolysis in BAT and core body temperature when subjected to cold treatment. Notably, Cidea-null mice are lean and resistant to diet-induced obesity and diabetes. Furthermore, we provide evidence that the role of Cidea in regulating thermogenesis, lipolysis and obesity may be mediated in part through its direct suppression of Ucp1 activity. Our data thus indicate a role for Cidea in regulating energy balance and adiposity.


 




All right reserved Center For Life Sciences