Abstract
Brown fat cells, freshly isolated from cold-acclimated hamsters and rats, did not respond to norepinephrine addition with the characteristic increase in O2 consumption (heat production) seen in cells from control animals. Incubation of these cells for 1 h in a Krebs-Ringer bicarbonate buffer, in the presence of 10 mM pyruvate, fully restored norepinephrine responsiveness. Cells treated in this way from cold-acclimated hamsters (a hibernator) increased the rate of O2 consumption after maximal norepinephrine stimulation as much as cells from control hamsters; norepinephrine-stimulated fatty acid release was unaltered, indicating that brown fat cells may partly be responsible for the increase in serum fatty acid level seen during arousal from hibernation. Preincubated cells from cold-acclimated rats (a nonhibernator) increased O2 consumption and fatty acid release as much as cells from control rats; in cold-acclimated rats brown fat may supply the circulation with fatty acids during cold stress. Cells from cold-acclimated animals were about 10 times less sensitive to norepinephrine than cells from control animals; this desensitization may be the result of a stimulated phosphodiesterase.

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