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Nature:CRTC3蛋白與肥胖癥有關

日期:2011-08-02 10:57:15

Nature:CRTC3蛋白與肥胖癥有關

“環狀AMP-響應蛋白CRTC3”(CREB-調控的轉錄共激發因子-3),被發現通過降低脂肪細胞中貝塔-腎上腺素能受體的信號作用,促進吃高脂肪食物的小鼠發生肥胖和產生胰島素抗性。CRTC3主要在脂肪組織中表達;缺少CRTC3的小鼠不會發生飲食誘導的肥胖,并能對胰島素保持敏感性。這項工作表明,CRTC3也許是肥胖癥形成中的一個早期信號,并且在II-型糖尿病中可能也是一個早期信號
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


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