Catecholamine sensitivity in brown fat cells from cold-acclimated hamsters and rats

1982 ◽  
Vol 242 (3) ◽  
pp. C250-C257 ◽  
Author(s):  
J. Nedergaard

Brown fat cells, freshly isolated from cold-acclimated hamsters and rats, did not respond to norepinephrine addition with the characteristic increase in oxygen consumption (heat production) seen in cells from control animals. However, 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 oxygen consumption after maximal norepinephrine stimulation as much as cells from control hamsters; also 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. Similarly, preincubated cells from cold-acclimated rats (a nonhibernator) increased oxygen consumption and fatty acid release as much as cells from control rats; this suggests that also in cold-acclimated rats brown fat may supply the circulation with fatty acids during cold stress. Cells from cold-acclimated animals were, however, about 10 times less sensitive to norepinephrine than cells from control animals; this desensitization may be the result of a stimulated phosphodiesterase.

1993 ◽  
Vol 265 (5) ◽  
pp. C1340-C1348 ◽  
Author(s):  
L. Unelius ◽  
G. Bronnikov ◽  
N. Mohell ◽  
J. Nedergaard

To investigate a possible physiological desensitization process for beta 3-adrenergic responses, the effect of cold acclimation of hamsters on adrenergically stimulated oxygen consumption of isolated brown fat cells was investigated. Cells were prepared from control and from cold-acclimated hamsters. In agreement with earlier findings, cells isolated from cold-acclimated hamsters responded to norepinephrine addition with a decreased sensitivity (approximately 10 times higher 50% effective concentration) and a decreased maximal rate of oxygen consumption compared with cells from control hamsters. When cells were stimulated with the general beta-adrenergic agonist isoprenaline or with the beta 3-selective agonists BRL-37344 or CGP-12177, a similarly desensitized response was observed, demonstrating that it was indeed a beta 3-adrenergic response that was functionally desensitized. However, when the mitochondria within the cells were directly stimulated with exogenous free fatty acids (palmitate or octanoate), no difference between cells from control and cold-acclimated animals was seen, indicating that a mediatory step must be desensitized. When the cells were stimulated with forskolin (to activate adenylyl cyclase) or with 8-bromoadenosine 3',5'-cyclic monophosphate, the desensitized response was still observed. At post-adenosine 3',5'-cyclic monophosphate levels, a desensitization was not evident. Cyclic nucleotide phosphodiesterase activity was increased in cells from cold-acclimated animals. It is therefore suggested that this increased activity of phosphodiesterase could be (at least partly) responsible for the physiologically induced desensitized responses observed here.(ABSTRACT TRUNCATED AT 250 WORDS)


2003 ◽  
Vol 278 (21) ◽  
pp. 18785-18790 ◽  
Author(s):  
Joan Tordjman ◽  
Geneviève Chauvet ◽  
Joëlle Quette ◽  
Elmus G. Beale ◽  
Claude Forest ◽  
...  

1999 ◽  
Vol 274 (26) ◽  
pp. 18243-18251 ◽  
Author(s):  
Vanessa Van Harmelen ◽  
Signy Reynisdottir ◽  
Katherine Cianflone ◽  
Eva Degerman ◽  
Johan Hoffstedt ◽  
...  

1966 ◽  
Vol 22 (2) ◽  
pp. 86-87 ◽  
Author(s):  
R. -J. Ho ◽  
B. Jeanrenaud ◽  
A. E. Renold

Sign in / Sign up

Export Citation Format

Share Document