The control of UCP1 is dissociated from that of PGC-1alpha or of mitochondriogenesis as revealed by a study using beta-less mouse brown adipocytes in culture |
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Authors: | Lehr Lorenz Canola Kriss Asensio Cedric Jimenez Maria Kuehne Françoise Giacobino Jean-Paul Muzzin Patrick |
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Affiliation: | Department of Cell Physiology and Metabolism, Centre Médical Universitaire, Geneva, Switzerland. lehr6@etu.unige.ch |
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Abstract: | In rodent brown adipose tissue, the beta-adrenergic signaling is believed, by an action on PGC-1alpha, to control UCP1 expression and mitochondriogenesis. We addressed this hypothesis using beta(1)/beta(2)/beta(3)-adrenoceptor knockout (beta-less) brown adipocytes in primary culture. In these cells: (a) proliferation and differentiation into multilocular cells were normal; (b) UCP1 mRNA expression was dramatically decreased (by 93%), whereas PGC-1alpha and mtTFA mRNA expressions were not; (c) UCP1, PGC-1alpha and COX IV protein expressions were decreased by 97%, 62% and 22%, respectively. Altogether the data show a dissociation between the control of UCP1, which is mostly beta-adrenoceptor-dependent and that of PGC-1alpha and of mitochondriogenesis which are not. |
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Keywords: | UCP1 PGC-1α Mitochondriogenesis β-less mice Brown adipocytes |
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