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The control of UCP1 is dissociated from that of PGC‐1α or of mitochondriogenesis as revealed by a study using β‐less mouse brown adipocytes in culture
Author(s) -
Lehr Lorenz,
Canola Kriss,
Asensio Cedric,
Jimenez Maria,
Kuehne Françoise,
Giacobino Jean-Paul,
Muzzin Patrick
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.07.037
Subject(s) - thermogenin , adipose tissue , tfam , messenger rna , endocrinology , medicine , brown adipose tissue , chemistry , microbiology and biotechnology , biology , mitochondrion , gene , biochemistry , mitochondrial biogenesis
In rodent brown adipose tissue, the β‐adrenergic signaling is believed, by an action on PGC‐1α, to control UCP1 expression and mitochondriogenesis. We addressed this hypothesis using β 1 /β 2 /β 3 ‐adrenoceptor knockout (β‐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‐1α and mtTFA mRNA expressions were not; (c) UCP1, PGC‐1α 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 β‐adrenoceptor‐dependent and that of PGC‐1α and of mitochondriogenesis which are not.

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