Journal
CELL METABOLISM
Volume 18, Issue 2, Pages 199-211Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2013.07.001
Keywords
-
Categories
Funding
- Spanish Ministry of Economy & Competitiveness [SAF2009-07172, SAF2012-31371, RD06/0020/0001, RD12/0036/0002, RYC-2008-02219, SAF2009-07049]
- Spanish Ministry of Economy & Competitiveness (CIBER de Fisiopatologia de la Obesidad y Nutricion) [BFU2011]
- Galician Autonomous Government
- European Union [ERC-2011-StG-OBESITY53-281408, 245009]
- European Regional Development Fund
Ask authors/readers for more resources
The role of the sympathetic nervous system, stress, and hypertension in metabolic syndrome and obesity remains unclear. To clarify this issue, we utilized genetically engineered mice showing chronic sympathoexcitation and hypertension due to lack of Vav3, a Rac1 activator. Here, we report that these animals develop metabolic syndrome under chow diet. However, they show protection from metabolic syndrome and obesity under fatty diets. These effects are elicited by alpha(1)-adrenergic- and diet-dependent metabolic changes in liver and the alpha(1)/beta(3) adrenergic-mediated stimulation of brown adipocyte thermogenesis. These responses seem to be engaged by the local action of noradrenaline in target tissues rather than by long-range effects of adrenaline. By contrast, they are not triggered by low parasympathetic drive or the hypertensive state present in Vav3-deficient mice. These results indicate that the sympathetic system plays divergent roles in the etiology of metabolic diseases depending on food regimen, sympathoexcitation source, and disease stage.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available