环状AMP-响应蛋白CRTC3”（CREB-调控的转录共激发因子-3），被发现通过降低脂肪细胞中贝塔-肾上腺素能受体的信号作用，促进吃高脂肪食物的小鼠发生肥胖和产生胰岛素抗性。CRTC3主要在脂肪组织中表达；缺少CRTC3的小鼠不会发生饮食诱导的肥胖，并能对胰岛素保持敏感性。这项工作表明，CRTC3也许是肥胖症形成中的一个早期信号，并且在II-型糖尿病中可能也是一个早期信号。（生物谷Bioon.com）

生物谷推荐原文出处：

Nature doi:10.1038/nature09564

CRTC3 links catecholamine signalling to energy balance

Youngsup Song,Judith Altarejos,Mark O. Goodarzi,Hiroshi Inoue,Xiuqing Guo,Rebecca Berdeaux,Jeong-Ho Kim,Jason Goode,Motoyuki Igata,Jose C. Paz,Meghan F. Hogan,Pankaj K. Singh,Naomi Goebel,Lili Vera,Nina Miller,Jinrui Cui,Michelle R. Jones,CHARGE Consortium,GIANT Consortium,Yii-Der I. Chen,Kent D. Taylor,Willa A. Hsueh,Jerome I. Rotter& Marc Montminy

The adipose-derived hormone leptin maintains energy balance in part through central nervous system-mediated increases in sympathetic outflow that enhance fat burning. Triggering of β-adrenergic receptors in adipocytes stimulates energy expenditure by cyclic AMP (cAMP)-dependent increases in lipolysis and fatty-acid oxidation. Although the mechanism is unclear, catecholamine signalling is thought to be disrupted in obesity, leading to the development of insulin resistance. Here we show that the cAMP response element binding (CREB) coactivator Crtc3 promotes obesity by attenuating β-adrenergic receptor signalling in adipose tissue. Crtc3 was activated in response to catecholamine signals, when it reduced adenyl cyclase activity by upregulating the expression of Rgs2, a GTPase-activating protein that also inhibits adenyl cyclase activity. As a common human CRTC3 variant with increased transcriptional activity is associated with adiposity in two distinct Mexican-American cohorts, these results suggest that adipocyte CRTC3 may play a role in the development of obesity in humans.