Is adrenergic innervation essential for maintenance of UCP in hamster BAT mitochondria?

The importance of the neural input for the maintenance of the mitochondrial content of the uncoupling protein (UCP) in hamster brown adipose tissue (BAT) was evaluated by unilateral surgical denervation and chemical sympathectomy with 6-hydroxydopamine. These interventions alone or in combination depleted (by 90-95%) the tissue catecholamine content to the same extent. Injections of 6-hydroxydopamine to hamsters caused reductions in BAT protein content but were without significant effect on [3H]GDP binding to isolated mitochondria or on the mitochondrial content of UCP measured by immunoassay. In contrast, surgical denervation, which had much less effect on BAT composition, caused a significant loss of UCP from the mitochondria. These results differ from those obtained in rats in which both chemical sympathectomy and surgical denervation caused a loss of UCP from the mitochondria. Norepinephrine infusion (with minipumps), which prevented denervation-induced BAT atrophy and reduction in mitochondrial content of UCP in rats, caused pronounced loss of tissue mass and mitochondrial proteins in hamsters and did not prevent the loss of UCP observed in mitochondria isolated from the denervated pad. Thus an intact innervation that may not be adrenergic is required for the expression of UCP in hamster BAT mitochondria.