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

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 β1/β2/β3-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.