The objectives of this study were to evaluate the rate at which brown adipose tissue (BAT) from mice
atrophies when its thermogenic activity is suppressed during fasting or exposure to a thermoneutral environment (33 degrees C) and whether such
atrophy is accompanied by loss from BAT mitochondria of "
thermogenin," the
GDP binding protein associated with the calorigenic
proton conductance pathway.
Atrophy of mouse BAT was characterized by rapid loss of
protein but unchanged tissue
DNA content. The rate of
protein loss varied from 2 to 6 mg
protein/day depending on the environmental and feeding status of the mice. In synchrony with tissue
protein loss, there was a marked reduction in the tissue content of
mitochondrial proteins and of
thermogenin, measured by immunoassay. However, the concentration of
thermogenin in isolated mitochondria was unchanged by fasting or exposure of the mice to 33 degrees C for 48 h. By contrast, marked reduction in [3H]
GDP binding to isolated mitochondria were observed after exposure of the mice to 33 degrees C. Mice acclimated at 4 but not those acclimated at 21 degrees C showed reduction in
GDP binding to isolated mitochondria during fasting. These results clearly indicate that changes in
purine nucleotide binding to isolated mitochondria can occur in the absence of changes in the mitochondrial concentration of
thermogenin. Thus rapid decrease in BAT thermogenic capacity (e.g., during fasting or 33 degrees C exposure) appears dependent on extensive loss of tissue
protein, probably whole mitochondria, rather than rapid and selective removal of
thermogenin from the mitochondria.