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, Consortium Charge, Consortium Giant, Yii- Der I. Chen, Kent D. Taylor, Willa A. Hsueh, Jerome I. Rotter and Marc Montminy ()
Additional contact information
Youngsup Song: The Salk Institute for Biological Studies
Judith Altarejos: The Salk Institute for Biological Studies
Mark O. Goodarzi: Diabetes and Metabolism, Cedars-Sinai Medical Center
Hiroshi Inoue: The Salk Institute for Biological Studies
Xiuqing Guo: Medical Genetics Institute, Cedars-Sinai Medical Center
Rebecca Berdeaux: The Salk Institute for Biological Studies
Jeong-Ho Kim: The Salk Institute for Biological Studies
Jason Goode: The Salk Institute for Biological Studies
Motoyuki Igata: The Salk Institute for Biological Studies
Jose C. Paz: The Salk Institute for Biological Studies
Meghan F. Hogan: The Salk Institute for Biological Studies
Pankaj K. Singh: The Salk Institute for Biological Studies
Naomi Goebel: The Salk Institute for Biological Studies
Lili Vera: The Salk Institute for Biological Studies
Nina Miller: The Salk Institute for Biological Studies
Jinrui Cui: Medical Genetics Institute, Cedars-Sinai Medical Center
Michelle R. Jones: Diabetes and Metabolism, Cedars-Sinai Medical Center
Yii- Der I. Chen: Medical Genetics Institute, Cedars-Sinai Medical Center
Kent D. Taylor: Medical Genetics Institute, Cedars-Sinai Medical Center
Willa A. Hsueh: Diabetes Research Center, Obesity and Lipids, Methodist Hospital Research Institute
Jerome I. Rotter: Medical Genetics Institute, Cedars-Sinai Medical Center
Marc Montminy: The Salk Institute for Biological Studies

Nature, 2010, vol. 468, issue 7326, 933-939

Abstract: Abstract 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.

Date: 2010
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DOI: 10.1038/nature09564

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