Cidea-deficient mice have lean phenotype and are resistant to obesity
Nature genetics volume 35 no. 1 pp 49 - 56
Zhihong Zhou1, Shen Yon Toh1, Zhengming Chen1, Ke Guo2, Chee Peng Ng3, Sathivel Ponniah4, Sheng-Cai Lin2, Wanjin Hong3 & Peng Li1, 5
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.
Full text:http://www.nature.com/cgi-taf/DynaPage.taf?file=/ng/journal/v35/n1/full/ng1225.html
