Key result
Continuous noradrenaline infusion in guinea pigs induces cold-adaptation changes, increasing uncoupling protein ~5-fold.
Simultaneous alpha- and beta-adrenergic stimulation is required to induce cold-adaptation-like changes and uncoupling protein expression in brown adipocytes of guinea pigs.
Leaves open noradrenaline's role in human brown fat adaptation; hypothesis-generating for adrenergic pathways, requiring clinical validation.
Continuous infusion of noradrenaline over the interscapular brown fat of guinea pigs maintained at thermoneutrality (28-32 degrees C) induces changes similar to those after cold-adaptation. (1) Multilocular fat droplets appear within the brown adipocytes. (2) The number of mitochondria per adipocyte and the total number of adipocytes both increase. (3) Noradrenaline addition to isolated adipocytes causes near maximal uncontrolled respiration. (4) The cells become more sensitive to fatty acid-induced uncoupling. (5) The tissue-specific uncoupling protein per mg of mitochondrial protein is increased 5-fold. Specific alpha- and beta-agonists were also chronically infused. (6) Separate infusion of phenylephrine or isoprenaline was not able to stimulate mitochondriogenesis or hyperplasia. (7) Adipocytes from these animals could not be uncoupled by acute noradrenaline. (8) Simultaneous chronic infusion of phenylephrine and isoprenaline reproduced the effects of chronic noradrenaline infusion.
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Cunningham et al. (1987) studied this question. Continuous infusion of noradrenaline vs. Specific alpha- and beta-agonists (phenylephrine or isoprenaline) was evaluated on Induction of functional uncoupling protein and changes in brown adipocytes. Continuous infusion of noradrenaline in guinea pigs induced changes similar to cold-adaptation, including a 5-fold increase in tissue-specific uncoupling protein per mg of mitochondrial protein.
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