Author
Listed:
- 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)
- CHARGE Consortium
- GIANT Consortium
- 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)
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.
Suggested Citation
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 & N, 2010.
"CRTC3 links catecholamine signalling to energy balance,"
Nature, Nature, vol. 468(7326), pages 933-939, December.
Handle:
RePEc:nat:nature:v:468:y:2010:i:7326:d:10.1038_nature09564
DOI: 10.1038/nature09564
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