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β-Adrenergic control of stearoyl-CoA desaturase 1 repression in relation to sympathoadrenal regulation of thermogenesis

  • Mainieri, Davide Department of Medicine/Physiology, University of Fribourg, Switzerland
  • Montani, Jean-Pierre Department of Medicine/Physiology, University of Fribourg, Switzerland
  • Seydoux, Josiane Department of Neuroscience, Centre Médical Universitaire, Geneva, Switzerland
  • Giacobino, J. P. Department of Medical Biochemistry, Centre Médical Universitaire, Geneva, Switzerland
  • Boss, O. Sirtris Pharmaceuticals Inc., Cambridge, USA
  • Dulloo, Abdul G. Department of Medicine/Physiology, University of Fribourg, Switzerland
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    27.06.2006
Published in:
  • International Journal of Obesity. - 2007, vol. 31, no. 2, p. 378–381
Thermogenesis
type 2 diabetes
sympathetic nervous system
catecholamines
English Mice lacking β-adrenoceptors, which mediate the thermogenic effects of norepinephrine and epinephrine, show diminished thermogenesis and high susceptibility to obesity, whereas mice lacking stearoyl-CoA desaturase 1 (SCD1), which catalyzes the synthesis of monounsaturated fatty acids, show enhanced thermogenesis and high resistance to obesity. In testing whether β-adrenergic control of thermogenesis might be mediated via repression of the SCD1 gene, we found that in mice lacking β-adrenoceptors, the gene expression of SCD1 is elevated in liver, skeletal muscle and white adipose tissue. In none of these tissues/organs, however, could a link be found between increased sympathetic nervous system activity and diminished SCD1 gene expression when thermogenesis is increased in response to diet or cold, nor is the SCD1 transcript repressed by the administration of epinephrine. Taken together, these studies suggest that the elevated SCD1 transcript in tissues of mice lacking β-adrenoceptors is not a direct effect of blunted β-adrenergic signalling, and that β-adrenergic control of SCD1 repression is unlikely to be a primary effector mechanism in sympathoadrenal regulation of thermogenesis. Whether approaches that target both SCD1 and molecular effectors of thermogenesis under β-adrenergic control might be more effective than targeting SCD1 alone are potential avenues for future research in obesity management.
Faculty
Faculté des sciences et de médecine
Department
Département de Médecine
Language
  • English
Classification
Biological sciences
License
License undefined
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Persistent URL
https://folia.unifr.ch/unifr/documents/300556
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