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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adipocytes / cytology
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Adipocytes / physiology*
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Adipose Tissue, Brown / cytology
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Adipose Tissue, Brown / physiology*
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Animals
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Base Sequence
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Blotting, Western
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Carrier Proteins / genetics
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Carrier Proteins / physiology*
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DNA Primers
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Ion Channels
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Membrane Proteins / genetics
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Membrane Proteins / physiology*
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Mice
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Mitochondrial Proteins
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
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Polymerase Chain Reaction
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RNA, Messenger / genetics
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Receptors, Adrenergic, beta / genetics
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Receptors, Adrenergic, beta / physiology*
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Trans-Activators / physiology*
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Transcription Factors
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Uncoupling Protein 1
Substances
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Carrier Proteins
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DNA Primers
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Ion Channels
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Membrane Proteins
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Mitochondrial Proteins
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
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Ppargc1a protein, mouse
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RNA, Messenger
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Receptors, Adrenergic, beta
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Trans-Activators
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Transcription Factors
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Ucp1 protein, mouse
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Uncoupling Protein 1